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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">cardiotomsk</journal-id><journal-title-group><journal-title xml:lang="ru">Сибирский журнал клинической и экспериментальной медицины</journal-title><trans-title-group xml:lang="en"><trans-title>Siberian Journal of Clinical and Experimental Medicine</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2713-2927</issn><issn pub-type="epub">2713-265X</issn><publisher><publisher-name>TSU publishing</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.29001/2073-8552-2016-31-3-7-15</article-id><article-id custom-type="elpub" pub-id-type="custom">cardiotomsk-221</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ОБЗОРЫ И ЛЕКЦИИ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEWS AND LECTURES</subject></subj-group></article-categories><title-group><article-title>С-JUN N-ТЕРМИНАЛЬНЫЕ КИНАЗЫ И ИХ МОДУЛЯТОРЫ ПРИ ИШЕМИЧЕСКИ– РЕПЕРФУЗИОННОМ ПОВРЕЖДЕНИИ МИОКАРДА (ОБЗОР ЛИТЕРАТУРЫ)</article-title><trans-title-group xml:lang="en"><trans-title>С-JUN N-TERMINAL KINASES AND THEIR MODULATORS IN MYOCARDIAL ISCHEMIA/REPERFUSION INJURY (REVIEW)</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Шведова</surname><given-names>М. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Shvedova</surname><given-names>M. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>канд. мед. наук, врач-хирург клиники госпитальной хирургии;</p><p>младший научный сотрудник,</p><p>634028, г. Томск, пр. Ленина, 4</p></bio><bio xml:lang="en"><p>Tomsk</p></bio><email xlink:type="simple">shvedovamv55@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Анфиногенова</surname><given-names>Я. Д.</given-names></name><name name-style="western" xml:lang="en"><surname>Anfinogenova</surname><given-names>Y.</given-names></name></name-alternatives><bio xml:lang="ru"><p>докт. мед. наук, ведущий научный сотрудник отделения популяционной кардиологии с группой научно-медицинской информации, патентоведения и международных связей;</p><p>научный сотрудник;</p><p>профессор кафедры нормальной физиологии,</p><p>634012, г. Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Tomsk</p></bio><email xlink:type="simple">ya@cardio-tomsk.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Попов</surname><given-names>С. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Popov</surname><given-names>S. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>докт. мед. наук, профессор, член-корреспондент РАН, заслуженный деятель науки РФ; директор,</p><p>634012, г. Томск, ул. Киевская, 111а</p></bio><email xlink:type="simple">psv@cardio-tomsk.ru</email><xref ref-type="aff" rid="aff-3"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Щепеткин</surname><given-names>И. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Shchepetkin</surname><given-names>I. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>ведущий научный сотрудник;</p><p>канд. мед. наук, старший научный сотрудник Отдела микробиологии и иммунологии, </p><p>960 Technology Blvd., Department of Microbiology and Immunology, Montana State University, Bozeman, Montana 59715, USA</p></bio><bio xml:lang="en"><p>Tomsk;</p><p>Bozeman, Montana, USA</p></bio><email xlink:type="simple">igor@montana.edu</email><xref ref-type="aff" rid="aff-4"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Аточин</surname><given-names>Д. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Atochin</surname><given-names>D. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>заведующий лабораторией изучения механизмов нейропротекции;</p><p>канд. биол. наук, Assistant Professor in Medicine, Cardiology Division, Cardiovascular Research Center,</p><p>149 13th Street, 4th Floor, Charlestown, MA 02129</p></bio><bio xml:lang="en"><p>Tomsk;</p><p>Charlestown, Massachusetts, USA</p></bio><email xlink:type="simple">atochin@cvrc.mgh.harvard.edu</email><xref ref-type="aff" rid="aff-5"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Федеральное государственное бюджетное образовательное учреждение высшего образования “Сибирский государственный медицинский университет” Министерства здравоохранения Российской Федерации;&#13;
Центр RASA в Томске, Федеральное государственное автономное образовательное учреждение высшего образования “Национальный исследовательский Томский политехнический университет”</institution><country>Россия</country></aff><aff xml:lang="en"><institution>RASA Center in Tomsk, Tomsk Polytechnic University;&#13;
Siberian State Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Научно-исследовательский институт кардиологии, Томский национальный исследовательский медицинский центр Российской академии наук;&#13;
Центр RASA в Томске, Федеральное государственное автономное образовательное учреждение высшего образования “Национальный исследовательский Томский политехнический университет” &#13;
Центр RASA ФГАОУ ВО НИ ТПУ; &#13;
Федеральное государственное бюджетное образовательное учреждение высшего образования “Сибирский государственный медицинский университет” Министерства здравоохранения Российской Федерации ФГБОУ ВО СибГМУ Минздрава России</institution><country>Россия</country></aff><aff xml:lang="en"><institution>RASA Center in Tomsk, Tomsk Polytechnic University;&#13;
Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences;&#13;
Siberian State Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-3"><aff xml:lang="ru"><institution>Научно-исследовательский институт кардиологии, Томский национальный исследовательский медицинский центр Российской академии наук</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-4"><aff xml:lang="ru"><institution>Центр RASA в Томске, Федеральное государственное автономное образовательное учреждение высшего образования “Национальный исследовательский Томский политехнический университет”;&#13;
Отдел микробиологии и иммунологии, университет штата Монтана</institution><country>Россия</country></aff><aff xml:lang="en"><institution>RASA Center in Tomsk, Tomsk Polytechnic University;&#13;
Department of Microbiology and Immunology, Montana State University</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-5"><aff xml:lang="ru"><institution>Центр RASA в Томске, Федеральное государственное автономное образовательное учреждение высшего образования “Национальный исследовательский Томский политехнический университет”;&#13;
Центр сердечно-сосудистых исследований и Отдел кардиологии, Главный госпиталь Массачусетса, Гарвардская медицинская школа</institution><country>Россия</country></aff><aff xml:lang="en"><institution>RASA Center in Tomsk, Tomsk Polytechnic University;&#13;
Cardiovascular Research Center, Cardiology Division, Massachusetts General Hospital, Harvard Medical School</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2016</year></pub-date><pub-date pub-type="epub"><day>04</day><month>11</month><year>2016</year></pub-date><volume>31</volume><issue>3</issue><fpage>7</fpage><lpage>15</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Шведова М.В., Анфиногенова Я.Д., Попов С.В., Щепеткин И.А., Аточин Д.Н., 2016</copyright-statement><copyright-year>2016</copyright-year><copyright-holder xml:lang="ru">Шведова М.В., Анфиногенова Я.Д., Попов С.В., Щепеткин И.А., Аточин Д.Н.</copyright-holder><copyright-holder xml:lang="en">Shvedova M.V., Anfinogenova Y., Popov S.V., Shchepetkin I.A., Atochin D.N.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.sibjcem.ru/jour/article/view/221">https://www.sibjcem.ru/jour/article/view/221</self-uri><abstract><p>Представлен обзор литературы, посвященный роли с Jun N терминальных киназ (JNK) в ишемически реперфу зионном повреждении миокарда. Дана классификация JNK, описаны их функции в сигнальныx механизмax, вовлеченныx в повреждение миокарда при ишемии и реперфузии. Авторы обсуждают биологические эффекты фармакологической модуляции JNK с использованием синтетических и природных соединений в эксперимен тальных моделях ишемически реперфузионного поражения миокарда. Подчеркивается роль JNK в механизмах ишемического пре и посткондиционирования сердца. Результаты экспериментальных исследований показыва ют, что JNK представляют собой потенциальные терапевтические мишени для защиты сердца от ишемически– реперфузионного повреждения. В то же время наличие многочисленных физиологических функций JNK не по зволяет системно использовать неспецифические ингибиторы этих ферментов с терапевтической целью. Авторы заключают, что актуальной задачей остается дальнейший поиск селективных ингибиторов JNK3.</p></abstract><trans-abstract xml:lang="en"><p>The article provides review of literature on the role of c Jun N terminal kinases (JNK) in ischemia/reperfusion injury of the myocardium. The classification of JNK is presented; JNK functions in signaling mechanisms are described in the context of ischemia/reperfusion injury. Authors discuss biological effects of pharmacological modulation of JNK by using synthetic and natural compounds in the models of myocardial ischemia/reperfusion. The role of JNK in the mechanisms of pre and postconditioning of the heart is highlighted. Results of experimental studies are demonstrated that JNK represent potential therapeutic targets for cardiac protection from ischemia/reperfusion injury. At the same time, the presence of multiple physiological JNK properties does not allow for systemic use of non specific JNK inhibitors for therapeutic purposes. Authors conclude that the actual problem is the further search for selective JNK3 inhibitors.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>апоптоз</kwd><kwd>c-Jun-N терминальная киназа</kwd><kwd>ингибитор JNK</kwd><kwd>ишемически–реперфузионное повреждение</kwd><kwd>миокард</kwd><kwd>терапевтическая мишень</kwd></kwd-group><kwd-group xml:lang="en"><kwd>apoptosis</kwd><kwd>c-Jun-N terminal kinase</kwd><kwd>JNK inhibitor</kwd><kwd>ischemia/reperfusion injury</kwd><kwd>myocardium</kwd><kwd>therapeutic target</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">государственное задание “Наука”</funding-statement></funding-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Влаопулос С., Зумпурлис В.С. JNK: ключевой модулятор внутриклеточной сигнальной системы // Биохимия. – 2004. – № 69(8). – С. 1038–1050.</mixed-citation><mixed-citation xml:lang="en">Влаопулос С., Зумпурлис В.С. JNK: ключевой модулятор внутриклеточной сигнальной системы // Биохимия. – 2004. – № 69(8). – С. 1038–1050.</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Зюзьков Г.Н., Жданов В.В., Удут Е.В. и др. Роль JNK и участие p53 в реализации ростового потенциала мезенхимных клеток предшественников в условиях in vitro // Бюллетень экспериментальной биологии и медицины. – 2015. – № 159(2). – С. 205–208.</mixed-citation><mixed-citation xml:lang="en">Зюзьков Г.Н., Жданов В.В., Удут Е.В. и др. Роль JNK и участие p53 в реализации ростового потенциала мезенхимных клеток предшественников в условиях in vitro // Бюллетень экспериментальной биологии и медицины. – 2015. – № 159(2). – С. 205–208.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Маслов Л.Н., Мрочек А.Г., Щепёткин И.А. и др. Роль протеинкиназ в формировании адаптивного феномена ишемического посткондиционирования сердца // Рос. физиологический журнал им. И.М. Сеченова. – 2013. – № 99(4). – С. 433–452.</mixed-citation><mixed-citation xml:lang="en">Маслов Л.Н., Мрочек А.Г., Щепёткин И.А. и др. Роль протеинкиназ в формировании адаптивного феномена ишемического посткондиционирования сердца // Рос. физиологический журнал им. И.М. Сеченова. – 2013. – № 99(4). – С. 433–452.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Рязанцева Н.В., Новицкий В.В., Часовских Н.Ю. и др. Роль редокс зависимых сигнальных систем в регуляции апоптоза при окислительном стрессе // Цитология. – 2009. – № 51(4). – С. 329–334.</mixed-citation><mixed-citation xml:lang="en">Рязанцева Н.В., Новицкий В.В., Часовских Н.Ю. и др. Роль редокс зависимых сигнальных систем в регуляции апоптоза при окислительном стрессе // Цитология. – 2009. – № 51(4). – С. 329–334.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Aoki H., Kang P.M., Hampe J. et al. Direct activation of mitochondrial apoptosis machinery by c Jun N terminal kinase in adult cardiac myocytes // J. Biol. Chem. – 2002. – Vol. 277(12). – P. 10244–10250.</mixed-citation><mixed-citation xml:lang="en">Aoki H., Kang P.M., Hampe J. et al. Direct activation of mitochondrial apoptosis machinery by c Jun N terminal kinase in adult cardiac myocytes // J. Biol. Chem. – 2002. – Vol. 277(12). – P. 10244–10250.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Armstrong S.C. Protein kinase activation and myocardial ischemia/reperfusion injury // Cardiovasc. Res. – 2004. – Vol. 61(3). – P. 427–436.</mixed-citation><mixed-citation xml:lang="en">Armstrong S.C. Protein kinase activation and myocardial ischemia/reperfusion injury // Cardiovasc. Res. – 2004. – Vol. 61(3). – P. 427–436.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Arslan F., Lai R.C., Smeets M.B. et al. Mesenchymal stem cell derived exosomes increase ATP levels, decrease oxidative stress and activate PI3K/Akt pathway to enhance myocardial viability and prevent adverse remodeling after myocardial ischemia/ reperfusion injury // Stem Cell Res. – 2013. – Vol. 10(3). – P. 301–312.</mixed-citation><mixed-citation xml:lang="en">Arslan F., Lai R.C., Smeets M.B. et al. Mesenchymal stem cell derived exosomes increase ATP levels, decrease oxidative stress and activate PI3K/Akt pathway to enhance myocardial viability and prevent adverse remodeling after myocardial ischemia/ reperfusion injury // Stem Cell Res. – 2013. – Vol. 10(3). – P. 301–312.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Atochin D.N., Schepetkin I.A., Khlebnikov A.I. et al. A novel dual NO donating oxime and c Jun N terminal kinase inhibitor protects against cerebral ischemia reperfusion injury in mice // Neurosci. Lett. – 2016. – Vol. 618. – P. 45–49.</mixed-citation><mixed-citation xml:lang="en">Atochin D.N., Schepetkin I.A., Khlebnikov A.I. et al. A novel dual NO donating oxime and c Jun N terminal kinase inhibitor protects against cerebral ischemia reperfusion injury in mice // Neurosci. Lett. – 2016. – Vol. 618. – P. 45–49.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Barancik M., Htun P., Schaper W. Okadaic acid and anisomycin are protective and stimulate the SAPK/JNK pathway // J. Cardiovasc. Pharmacol. – 1999. – Vol. 34(2). – P. 182–190.</mixed-citation><mixed-citation xml:lang="en">Barancik M., Htun P., Schaper W. Okadaic acid and anisomycin are protective and stimulate the SAPK/JNK pathway // J. Cardiovasc. Pharmacol. – 1999. – Vol. 34(2). – P. 182–190.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Becatti M., Taddei N., Cecchi C. et al. SIRT1 modulates MAPK pathways in ischemic reperfused cardiomyocytes // Cell. Mol. Life Sci. – 2012. – Vol. 69(13). – P. 2245–2260.</mixed-citation><mixed-citation xml:lang="en">Becatti M., Taddei N., Cecchi C. et al. SIRT1 modulates MAPK pathways in ischemic reperfused cardiomyocytes // Cell. Mol. Life Sci. – 2012. – Vol. 69(13). – P. 2245–2260.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Bode A.M., Dong Z. The functional contrariety of JNK // Mol. Carcinog. – 2007. – Vol. 46(8). – P. 591–598.</mixed-citation><mixed-citation xml:lang="en">Bode A.M., Dong Z. The functional contrariety of JNK // Mol. Carcinog. – 2007. – Vol. 46(8). – P. 591–598.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Bogoyevitch M.A., Kobe B. Uses for JNK: the many and varied substrates of the c-Jun-N-terminal kinases // Microbiol. Mol. Biol. Rev. – 2006. – Vol. 70(4). – P. 1061–1095.</mixed-citation><mixed-citation xml:lang="en">Bogoyevitch M.A., Kobe B. Uses for JNK: the many and varied substrates of the c-Jun-N-terminal kinases // Microbiol. Mol. Biol. Rev. – 2006. – Vol. 70(4). – P. 1061–1095.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Chambers J.W., Pachori A., Howard S. et al. Inhibition of JNK mitochondrial localization and signaling is protective against ischemia/reperfusion injury in rats // J. Biol. Chem. – 2013. – Vol. 288(6). – P. 4000–4011.</mixed-citation><mixed-citation xml:lang="en">Chambers J.W., Pachori A., Howard S. et al. Inhibition of JNK mitochondrial localization and signaling is protective against ischemia/reperfusion injury in rats // J. Biol. Chem. – 2013. – Vol. 288(6). – P. 4000–4011.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Chaudhury H., Zakkar M., Boyle J. et al. C-Jun-N terminal kinase primes endothelial cells at atheroprone sites for apoptosis // Arterioscler. Thromb. Vasc. Biol. – 2010. – Vol. 30(3). – P. 546–553.</mixed-citation><mixed-citation xml:lang="en">Chaudhury H., Zakkar M., Boyle J. et al. C-Jun-N terminal kinase primes endothelial cells at atheroprone sites for apoptosis // Arterioscler. Thromb. Vasc. Biol. – 2010. – Vol. 30(3). – P. 546–553.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Chen Y.C., Jinn T.R., Chung T.Y. et al. Magnesium lithospermate B extracted from Salvia miltiorrhiza elevates intracellular Ca2+ level in SH SY5Y cells // Acta Pharmacol. Sin. – 2010. – Vol. 31(8). – P. 923–929.</mixed-citation><mixed-citation xml:lang="en">Chen Y.C., Jinn T.R., Chung T.Y. et al. Magnesium lithospermate B extracted from Salvia miltiorrhiza elevates intracellular Ca2+ level in SH SY5Y cells // Acta Pharmacol. Sin. – 2010. – Vol. 31(8). – P. 923–929.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Clerk A., Fuller S.J., Michael A. et al. Stimulation of “stress-regulated” mitogen-activated protein kinases (stress-activated protein kinases/c-Jun-N-terminal kinases and p38 mitogen-activated protein kinases) in perfused rat hearts by oxidative and other stresses // J. Biol. Chem. – 1998. – Vol. 273(13). – P. 7228–7234.</mixed-citation><mixed-citation xml:lang="en">Clerk A., Fuller S.J., Michael A. et al. Stimulation of “stress-regulated” mitogen-activated protein kinases (stress-activated protein kinases/c-Jun-N-terminal kinases and p38 mitogen-activated protein kinases) in perfused rat hearts by oxidative and other stresses // J. Biol. Chem. – 1998. – Vol. 273(13). – P. 7228–7234.</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Dougherty C.J., Kubasiak L.A., Frazier D.P. et al. Mitochondrial signals initiate the activation of c Jun N terminal kinase (JNK) by hypoxia-reoxygenation // FASEB J. – 2004. – Vol. 18(10). – P. 1060–1070.</mixed-citation><mixed-citation xml:lang="en">Dougherty C.J., Kubasiak L.A., Frazier D.P. et al. Mitochondrial signals initiate the activation of c Jun N terminal kinase (JNK) by hypoxia-reoxygenation // FASEB J. – 2004. – Vol. 18(10). – P. 1060–1070.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Dougherty C.J., Kubasiak L.A., Prentice H. et al. Activation of c-Jun N-terminal kinase promotes survival of cardiac myocytes after oxidative stress // Biochem. J. – 2002. – Vol. 362 (Pt. 3). – P. 561–571.</mixed-citation><mixed-citation xml:lang="en">Dougherty C.J., Kubasiak L.A., Prentice H. et al. Activation of c-Jun N-terminal kinase promotes survival of cardiac myocytes after oxidative stress // Biochem. J. – 2002. – Vol. 362 (Pt. 3). – P. 561–571.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Duplain H. Salvage of ischemic myocardium: a focus on JNK // Adv. Exp. Med. Biol. – 2006. – Vol. 588. – P. 157–164.</mixed-citation><mixed-citation xml:lang="en">Duplain H. Salvage of ischemic myocardium: a focus on JNK // Adv. Exp. Med. Biol. – 2006. – Vol. 588. – P. 157–164.</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Engelbrecht A.M., Niesler C., Page C. et al. P38 and JNK have distinct regulatory functions on the development of apoptosis during simulated ischaemia and reperfusion in neonatal cardiomyocytes // Basic Res. Cardiol. – 2004. – Vol. 99(5). – P. 338–350.</mixed-citation><mixed-citation xml:lang="en">Engelbrecht A.M., Niesler C., Page C. et al. P38 and JNK have distinct regulatory functions on the development of apoptosis during simulated ischaemia and reperfusion in neonatal cardiomyocytes // Basic Res. Cardiol. – 2004. – Vol. 99(5). – P. 338–350.</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Ferrandi C., Ballerio R., Gaillard P. et al. Inhibition of c-Jun N-terminal kinase decreases cardiomyocyte apoptosis and infarct size after myocardial ischemia and reperfusion in anaesthetized rats // Br. J. Pharmacol. – 2004. – Vol. 142(6). – P. 953–960.</mixed-citation><mixed-citation xml:lang="en">Ferrandi C., Ballerio R., Gaillard P. et al. Inhibition of c-Jun N-terminal kinase decreases cardiomyocyte apoptosis and infarct size after myocardial ischemia and reperfusion in anaesthetized rats // Br. J. Pharmacol. – 2004. – Vol. 142(6). – P. 953–960.</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Frazier D.P., Wilson A., Dougherty C.J. et al. PKC alpha and TAK-1 are intermediates in the activation of c-Jun NH2 terminal kinase by hypoxia reoxygenation // Am. J. Physiol. Heart Circ. Physiol. – 2007. – Vol. 292(4). – P. H1675–1684.</mixed-citation><mixed-citation xml:lang="en">Frazier D.P., Wilson A., Dougherty C.J. et al. PKC alpha and TAK-1 are intermediates in the activation of c-Jun NH2 terminal kinase by hypoxia reoxygenation // Am. J. Physiol. Heart Circ. Physiol. – 2007. – Vol. 292(4). – P. H1675–1684.</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Fryer R.M., Patel H.H., Hsu A.K. et al. Stress activated protein-kinase phosphorylation during cardioprotection in the ischemic myocardium // Am. J. Physiol. Heart. Circ. Physiol. – 2001. – Vol. 281(3). – P. H1184–1192.</mixed-citation><mixed-citation xml:lang="en">Fryer R.M., Patel H.H., Hsu A.K. et al. Stress activated protein-kinase phosphorylation during cardioprotection in the ischemic myocardium // Am. J. Physiol. Heart. Circ. Physiol. – 2001. – Vol. 281(3). – P. H1184–1192.</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Gehringer M., Muth F., Koch P., Laufer S.A. c-Jun N-terminal kinase inhibitors: a patent review (2010–2014) // Expert Opin. Ther. Pat. – 2015. – Vol. 25(8). – P. 849–872.</mixed-citation><mixed-citation xml:lang="en">Gehringer M., Muth F., Koch P., Laufer S.A. c-Jun N-terminal kinase inhibitors: a patent review (2010–2014) // Expert Opin. Ther. Pat. – 2015. – Vol. 25(8). – P. 849–872.</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Gupta S., Barrett T., Whitmarsh A.J. et al. Selective interaction of JNK protein kinase isoforms with transcription factors // The EMBO Journal. – 1996. – Vol. 15(11). – P. 2760–2770.</mixed-citation><mixed-citation xml:lang="en">Gupta S., Barrett T., Whitmarsh A.J. et al. Selective interaction of JNK protein kinase isoforms with transcription factors // The EMBO Journal. – 1996. – Vol. 15(11). – P. 2760–2770.</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Hausenloy D.J., Yellon D.M. Survival kinases in ischemic preconditioning and postconditioning // Cardiovasc. Res. – 2006. – Vol. 70(2). – P. 240–253.</mixed-citation><mixed-citation xml:lang="en">Hausenloy D.J., Yellon D.M. Survival kinases in ischemic preconditioning and postconditioning // Cardiovasc. Res. – 2006. – Vol. 70(2). – P. 240–253.</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Hausenloy D.J., Yellon D.M. Preconditioning and postconditioning: united at reperfusion // Pharmacol. Ther. – 2007. – Vol. 116(2). – P. 173–191.</mixed-citation><mixed-citation xml:lang="en">Hausenloy D.J., Yellon D.M. Preconditioning and postconditioning: united at reperfusion // Pharmacol. Ther. – 2007. – Vol. 116(2). – P. 173–191.</mixed-citation></citation-alternatives></ref><ref id="cit28"><label>28</label><citation-alternatives><mixed-citation xml:lang="ru">He H., Li H.L., Lin A. et al. Activation of the JNK pathway is important for cardiomyocyte death in response to simulated ischemia // Cell Death Differ. – 1999. – Vol. 6(10). – P. 987–991.</mixed-citation><mixed-citation xml:lang="en">He H., Li H.L., Lin A. et al. Activation of the JNK pathway is important for cardiomyocyte death in response to simulated ischemia // Cell Death Differ. – 1999. – Vol. 6(10). – P. 987–991.</mixed-citation></citation-alternatives></ref><ref id="cit29"><label>29</label><citation-alternatives><mixed-citation xml:lang="ru">Hreniuk D., Garay M., Gaarde W. et al. Inhibition of c-Jun N-terminal kinase 1, but not c-Jun N-terminal kinase 2, suppresses apoptosis induced by ischemia/reoxygenation in rat cardiac myocytes // Mol. Pharmacol. – 2001. – Vol. 59(4). — P. 867–874.</mixed-citation><mixed-citation xml:lang="en">Hreniuk D., Garay M., Gaarde W. et al. Inhibition of c-Jun N-terminal kinase 1, but not c-Jun N-terminal kinase 2, suppresses apoptosis induced by ischemia/reoxygenation in rat cardiac myocytes // Mol. Pharmacol. – 2001. – Vol. 59(4). — P. 867–874.</mixed-citation></citation-alternatives></ref><ref id="cit30"><label>30</label><citation-alternatives><mixed-citation xml:lang="ru">Ip Y.T., Davis R.J. Signal transduction by the c-Jun N-terminal kinase (JNK) – from inflammation to development // Curr. Opin. Cell Biol. – 1998. – Vol. 10(2). – P. 205–219.</mixed-citation><mixed-citation xml:lang="en">Ip Y.T., Davis R.J. Signal transduction by the c-Jun N-terminal kinase (JNK) – from inflammation to development // Curr. Opin. Cell Biol. – 1998. – Vol. 10(2). – P. 205–219.</mixed-citation></citation-alternatives></ref><ref id="cit31"><label>31</label><citation-alternatives><mixed-citation xml:lang="ru">Irving E.A., Bamford M. Role of mitogen and stress-activated kinases in ischemic injury // J. Cereb. Blood Flow Metab. – 2002. – Vol. 22(6). – P. 631–647.</mixed-citation><mixed-citation xml:lang="en">Irving E.A., Bamford M. Role of mitogen and stress-activated kinases in ischemic injury // J. Cereb. Blood Flow Metab. – 2002. – Vol. 22(6). – P. 631–647.</mixed-citation></citation-alternatives></ref><ref id="cit32"><label>32</label><citation-alternatives><mixed-citation xml:lang="ru">Jang S., Javadov S. Inhibition of JNK aggravates the recovery of rat hearts after global ischemia: the role of mitochondrial JNK // PLoS One. – 2014. – Vol. 9(11). – P. e113526.</mixed-citation><mixed-citation xml:lang="en">Jang S., Javadov S. Inhibition of JNK aggravates the recovery of rat hearts after global ischemia: the role of mitochondrial JNK // PLoS One. – 2014. – Vol. 9(11). – P. e113526.</mixed-citation></citation-alternatives></ref><ref id="cit33"><label>33</label><citation-alternatives><mixed-citation xml:lang="ru">Javadov S., Jang S., Agostini B. Crosstalk between mitogen-activated protein kinases and mitochondria in cardiac diseases: therapeutic perspectives // Pharmacol. Ther. – 2014. – Vol. 144(2). – P. 202–225.</mixed-citation><mixed-citation xml:lang="en">Javadov S., Jang S., Agostini B. Crosstalk between mitogen-activated protein kinases and mitochondria in cardiac diseases: therapeutic perspectives // Pharmacol. Ther. – 2014. – Vol. 144(2). – P. 202–225.</mixed-citation></citation-alternatives></ref><ref id="cit34"><label>34</label><citation-alternatives><mixed-citation xml:lang="ru">Johnson G.L., Nakamura K. The c-jun kinase/stress-activated pathway: regulation, function and role in human disease // Biochim. Biophys. Acta. – 2007. – Vol. 1773(8). – P. 1341–1348.</mixed-citation><mixed-citation xml:lang="en">Johnson G.L., Nakamura K. The c-jun kinase/stress-activated pathway: regulation, function and role in human disease // Biochim. Biophys. Acta. – 2007. – Vol. 1773(8). – P. 1341–1348.</mixed-citation></citation-alternatives></ref><ref id="cit35"><label>35</label><citation-alternatives><mixed-citation xml:lang="ru">Kaiser R.A., Liang Q., Bueno O. et al. Genetic inhibition or activation of JNK1/2 protects the myocardium from ischemia–reperfusion induced cell death in vivo // J. Biol. Chem. – 2005. – Vol. 280(38). – P. 32602–32608.</mixed-citation><mixed-citation xml:lang="en">Kaiser R.A., Liang Q., Bueno O. et al. Genetic inhibition or activation of JNK1/2 protects the myocardium from ischemia–reperfusion induced cell death in vivo // J. Biol. Chem. – 2005. – Vol. 280(38). – P. 32602–32608.</mixed-citation></citation-alternatives></ref><ref id="cit36"><label>36</label><citation-alternatives><mixed-citation xml:lang="ru">Khalid S., Drasche A., Thurner M. et al. c-Jun N-terminal kinase (JNK) phosphorylation of serine 36 is critical for p66Shc activation // Sci. Rep. – 2016. – Vol. 6. – P. 20930.</mixed-citation><mixed-citation xml:lang="en">Khalid S., Drasche A., Thurner M. et al. c-Jun N-terminal kinase (JNK) phosphorylation of serine 36 is critical for p66Shc activation // Sci. Rep. – 2016. – Vol. 6. – P. 20930.</mixed-citation></citation-alternatives></ref><ref id="cit37"><label>37</label><citation-alternatives><mixed-citation xml:lang="ru">Khandoudi N., Delerive P., Berrebi-Bertrand I. et al. Rosiglitazone, a peroxisome proliferator activated receptor-gamma, inhibits the Jun NH(2) terminal kinase/activating protein 1 pathway and protects the heart from ischemia/reperfusion injury // Diabetes. – 2002. – Vol. 51(5). – P. 1507–1514.</mixed-citation><mixed-citation xml:lang="en">Khandoudi N., Delerive P., Berrebi-Bertrand I. et al. Rosiglitazone, a peroxisome proliferator activated receptor-gamma, inhibits the Jun NH(2) terminal kinase/activating protein 1 pathway and protects the heart from ischemia/reperfusion injury // Diabetes. – 2002. – Vol. 51(5). – P. 1507–1514.</mixed-citation></citation-alternatives></ref><ref id="cit38"><label>38</label><citation-alternatives><mixed-citation xml:lang="ru">Knight R.J., Buxton D.B. Stimulation of c-Jun kinase and mitogen-activated protein kinase by ischemia and reperfusion in the perfused rat heart // Biochem. Biophys. Res. Commun. – 1996. – Vol. 218(1). – P. 83–88.</mixed-citation><mixed-citation xml:lang="en">Knight R.J., Buxton D.B. Stimulation of c-Jun kinase and mitogen-activated protein kinase by ischemia and reperfusion in the perfused rat heart // Biochem. Biophys. Res. Commun. – 1996. – Vol. 218(1). – P. 83–88.</mixed-citation></citation-alternatives></ref><ref id="cit39"><label>39</label><citation-alternatives><mixed-citation xml:lang="ru">Laderoute K.R., Webster K.A. Hypoxia/reoxygenation stimulates Jun kinase activity through redox signaling in cardiac myocytes // Circ. Res. – 1997. – Vol. 80(3). – P. 336–344.</mixed-citation><mixed-citation xml:lang="en">Laderoute K.R., Webster K.A. Hypoxia/reoxygenation stimulates Jun kinase activity through redox signaling in cardiac myocytes // Circ. Res. – 1997. – Vol. 80(3). – P. 336–344.</mixed-citation></citation-alternatives></ref><ref id="cit40"><label>40</label><citation-alternatives><mixed-citation xml:lang="ru">Li H.H., Du J., Fan Y.N. et al. The ubiquitin ligase MuRF1 protects against cardiac ischemia/reperfusion injury by its proteasome-dependent degradation of phospho c-Jun // Am. J. Pathol. – 2011. – Vol. 178(3). – P. 1043–1058.</mixed-citation><mixed-citation xml:lang="en">Li H.H., Du J., Fan Y.N. et al. The ubiquitin ligase MuRF1 protects against cardiac ischemia/reperfusion injury by its proteasome-dependent degradation of phospho c-Jun // Am. J. Pathol. – 2011. – Vol. 178(3). – P. 1043–1058.</mixed-citation></citation-alternatives></ref><ref id="cit41"><label>41</label><citation-alternatives><mixed-citation xml:lang="ru">Li C., Gao Y., Tian J. et al. Sophocarpine administration preserves myocardial function from ischemia reperfusion in rats via NF-кB inactivation // J. Ethnopharmacol. – 2011. – Vol. 135(3). – P. 620–625.</mixed-citation><mixed-citation xml:lang="en">Li C., Gao Y., Tian J. et al. Sophocarpine administration preserves myocardial function from ischemia reperfusion in rats via NF-кB inactivation // J. Ethnopharmacol. – 2011. – Vol. 135(3). – P. 620–625.</mixed-citation></citation-alternatives></ref><ref id="cit42"><label>42</label><citation-alternatives><mixed-citation xml:lang="ru">Li X.M., Ma Y.T., Yang Y.N. et al. Ischemic postconditioning protects hypertrophic myocardium by ERK1/2 signaling pathway: experiment with mice // Zhonghua Yi Xue Za Zhi. – 2009. – Vol. 89(12). – P. 846–850.</mixed-citation><mixed-citation xml:lang="en">Li X.M., Ma Y.T., Yang Y.N. et al. Ischemic postconditioning protects hypertrophic myocardium by ERK1/2 signaling pathway: experiment with mice // Zhonghua Yi Xue Za Zhi. – 2009. – Vol. 89(12). – P. 846–850.</mixed-citation></citation-alternatives></ref><ref id="cit43"><label>43</label><citation-alternatives><mixed-citation xml:lang="ru">Li C., Wang T., Zhang C. et al. Quercetin attenuates cardiomyocyte apoptosis via inhibition of JNK and p38 mitogen activated protein kinase signaling pathways // Gene. – 2016. – Vol. 577(2). – P. 275–280.</mixed-citation><mixed-citation xml:lang="en">Li C., Wang T., Zhang C. et al. Quercetin attenuates cardiomyocyte apoptosis via inhibition of JNK and p38 mitogen activated protein kinase signaling pathways // Gene. – 2016. – Vol. 577(2). – P. 275–280.</mixed-citation></citation-alternatives></ref><ref id="cit44"><label>44</label><citation-alternatives><mixed-citation xml:lang="ru">Liu Q., Wang J., Liang Q. et al. Sparstolonin B attenuates hypoxia-reoxygenation induced cardiomyocyte inflammation // Exp. Biol. Med. (Maywood). – 2014. – Vol. 239(3). – P. 376–384.</mixed-citation><mixed-citation xml:lang="en">Liu Q., Wang J., Liang Q. et al. Sparstolonin B attenuates hypoxia-reoxygenation induced cardiomyocyte inflammation // Exp. Biol. Med. (Maywood). – 2014. – Vol. 239(3). – P. 376–384.</mixed-citation></citation-alternatives></ref><ref id="cit45"><label>45</label><citation-alternatives><mixed-citation xml:lang="ru">Liu X., Xu F., Fu Y. et al. Calreticulin induces delayed cardioprotection through mitogen</mixed-citation><mixed-citation xml:lang="en">Liu X., Xu F., Fu Y. et al. Calreticulin induces delayed cardioprotection through mitogen</mixed-citation></citation-alternatives></ref><ref id="cit46"><label>46</label><citation-alternatives><mixed-citation xml:lang="ru">activated protein kinases // Proteomics. – 2006. – Vol. 6(13). – P. 3792–3800.</mixed-citation><mixed-citation xml:lang="en">activated protein kinases // Proteomics. – 2006. – Vol. 6(13). – P. 3792–3800.</mixed-citation></citation-alternatives></ref><ref id="cit47"><label>47</label><citation-alternatives><mixed-citation xml:lang="ru">Liu H.T., Zhang H.F., Si R. et al. Insulin protects isolated hearts from ischemia/reperfusion injury: cross talk between PI3-K/Akt and JNKs // Acta Physiol. Sin. – 2007. – Vol. 59(5). – P. 651–659.</mixed-citation><mixed-citation xml:lang="en">Liu H.T., Zhang H.F., Si R. et al. Insulin protects isolated hearts from ischemia/reperfusion injury: cross talk between PI3-K/Akt and JNKs // Acta Physiol. Sin. – 2007. – Vol. 59(5). – P. 651–659.</mixed-citation></citation-alternatives></ref><ref id="cit48"><label>48</label><citation-alternatives><mixed-citation xml:lang="ru">Liu X.H., Zhang Z.Y., Sun S. et al. Ischemic postconditioning protects myocardium from ischemia/reperfusion injury through attenuating endoplasmic reticulum stress // Shock. – 2008. – Vol. 30(4). – P. 422–427.</mixed-citation><mixed-citation xml:lang="en">Liu X.H., Zhang Z.Y., Sun S. et al. Ischemic postconditioning protects myocardium from ischemia/reperfusion injury through attenuating endoplasmic reticulum stress // Shock. – 2008. – Vol. 30(4). – P. 422–427.</mixed-citation></citation-alternatives></ref><ref id="cit49"><label>49</label><citation-alternatives><mixed-citation xml:lang="ru">Messoussi A., Feneyrolles C., Bros A. et al. Recent progress in the design, study, and development of c-Jun N-terminal kinase inhibitors as anticancer agents // Chem. Biol. – 2014. – Vol. 21(11). – P. 1433–1443.</mixed-citation><mixed-citation xml:lang="en">Messoussi A., Feneyrolles C., Bros A. et al. Recent progress in the design, study, and development of c-Jun N-terminal kinase inhibitors as anticancer agents // Chem. Biol. – 2014. – Vol. 21(11). – P. 1433–1443.</mixed-citation></citation-alternatives></ref><ref id="cit50"><label>50</label><citation-alternatives><mixed-citation xml:lang="ru">Milano G., Morel S., Bonny C. et al. A peptide inhibitor of c-Jun NH2-terminal kinase reduces myocardial ischemia reperfusion injury and infarct size in vivo // Am. J. Physiol. Heart Circ. Physiol. – 2007. – Vol. 292(4). – P. H1828–1835.</mixed-citation><mixed-citation xml:lang="en">Milano G., Morel S., Bonny C. et al. A peptide inhibitor of c-Jun NH2-terminal kinase reduces myocardial ischemia reperfusion injury and infarct size in vivo // Am. J. Physiol. Heart Circ. Physiol. – 2007. – Vol. 292(4). – P. H1828–1835.</mixed-citation></citation-alternatives></ref><ref id="cit51"><label>51</label><citation-alternatives><mixed-citation xml:lang="ru">Morrison A., Yan X., Tong C. et al. Acute rosiglitazone treatment is cardioprotective against ischemia reperfusion injury by modulating AMPK, Akt, and JNK signaling in nondiabetic mice // Am. J. Physiol. Heart Circ. Physiol. – 2011. – Vol. 301(3). – P. H895–902.</mixed-citation><mixed-citation xml:lang="en">Morrison A., Yan X., Tong C. et al. Acute rosiglitazone treatment is cardioprotective against ischemia reperfusion injury by modulating AMPK, Akt, and JNK signaling in nondiabetic mice // Am. J. Physiol. Heart Circ. Physiol. – 2011. – Vol. 301(3). – P. H895–902.</mixed-citation></citation-alternatives></ref><ref id="cit52"><label>52</label><citation-alternatives><mixed-citation xml:lang="ru">Nakano A., Baines C.P., Kim S.O. et al. Ischemic preconditioning activates MAPKAPK2 in the isolated rabbit heart: evidence for involvement of p38 MAPK // Circ. Res. – 2000. – Vol. 86(2). – P. 144–151.</mixed-citation><mixed-citation xml:lang="en">Nakano A., Baines C.P., Kim S.O. et al. Ischemic preconditioning activates MAPKAPK2 in the isolated rabbit heart: evidence for involvement of p38 MAPK // Circ. Res. – 2000. – Vol. 86(2). – P. 144–151.</mixed-citation></citation-alternatives></ref><ref id="cit53"><label>53</label><citation-alternatives><mixed-citation xml:lang="ru">Nijboer C.H., van der Kooij M.A., van Bel F. et al. Inhibition of the JNK/AP-1 pathway reduces neuronal death and improves behavioral outcome after neonatal hypoxic ischemic brain injury // Brain Behav. Immun. – 2010. – Vol. 24(5). – P. 812– 821.</mixed-citation><mixed-citation xml:lang="en">Nijboer C.H., van der Kooij M.A., van Bel F. et al. Inhibition of the JNK/AP-1 pathway reduces neuronal death and improves behavioral outcome after neonatal hypoxic ischemic brain injury // Brain Behav. Immun. – 2010. – Vol. 24(5). – P. 812– 821.</mixed-citation></citation-alternatives></ref><ref id="cit54"><label>54</label><citation-alternatives><mixed-citation xml:lang="ru">Oshikawa J., Kim S.J., Furuta E. et al. Novel role of p66Shc in ROS-dependent VEGF signaling and angiogenesis in endothelial cells // Am. J. Physiol. Heart Circ. Physiol. – 2012. – Vol. 302(3). – P. H724–732.</mixed-citation><mixed-citation xml:lang="en">Oshikawa J., Kim S.J., Furuta E. et al. Novel role of p66Shc in ROS-dependent VEGF signaling and angiogenesis in endothelial cells // Am. J. Physiol. Heart Circ. Physiol. – 2012. – Vol. 302(3). – P. H724–732.</mixed-citation></citation-alternatives></ref><ref id="cit55"><label>55</label><citation-alternatives><mixed-citation xml:lang="ru">Ping P., Zhang J., Huang S. et al. PKC-dependent activation of p46/p54 JNKs during ischemic preconditioning in conscious rabbits // Am. J. Physiol. – 1999. – Vol. 277(5 Pt. 2). – P. H1771–1785.</mixed-citation><mixed-citation xml:lang="en">Ping P., Zhang J., Huang S. et al. PKC-dependent activation of p46/p54 JNKs during ischemic preconditioning in conscious rabbits // Am. J. Physiol. – 1999. – Vol. 277(5 Pt. 2). – P. H1771–1785.</mixed-citation></citation-alternatives></ref><ref id="cit56"><label>56</label><citation-alternatives><mixed-citation xml:lang="ru">Qi D., Hu X., Wu X. et al. Cardiac macrophage migration inhibitory factor inhibits JNK pathway activation and injury during ischemia/reperfusion // J. Clin. Invest. – 2009. – Vol. 119(12). – P. 3807–3816.</mixed-citation><mixed-citation xml:lang="en">Qi D., Hu X., Wu X. et al. Cardiac macrophage migration inhibitory factor inhibits JNK pathway activation and injury during ischemia/reperfusion // J. Clin. Invest. – 2009. – Vol. 119(12). – P. 3807–3816.</mixed-citation></citation-alternatives></ref><ref id="cit57"><label>57</label><citation-alternatives><mixed-citation xml:lang="ru">Rose B.A., Force T., Wang Y. Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale // Physiol. Rev. – 2010. – Vol. 90(4). – P. 1507–1546.</mixed-citation><mixed-citation xml:lang="en">Rose B.A., Force T., Wang Y. Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale // Physiol. Rev. – 2010. – Vol. 90(4). – P. 1507–1546.</mixed-citation></citation-alternatives></ref><ref id="cit58"><label>58</label><citation-alternatives><mixed-citation xml:lang="ru">Sato M., Bagchi D., Tosaki A. et al. Grape seed proanthocyanidin reduces cardiomyocyte apoptosis by inhibiting ischemia/reperfusion induced activation of JNK-1 and C-JUN // Free Radic. Biol. Med. – 2001. – Vol. 31(6). – P. 729–737.</mixed-citation><mixed-citation xml:lang="en">Sato M., Bagchi D., Tosaki A. et al. Grape seed proanthocyanidin reduces cardiomyocyte apoptosis by inhibiting ischemia/reperfusion induced activation of JNK-1 and C-JUN // Free Radic. Biol. Med. – 2001. – Vol. 31(6). – P. 729–737.</mixed-citation></citation-alternatives></ref><ref id="cit59"><label>59</label><citation-alternatives><mixed-citation xml:lang="ru">Shang L., Ananthakrishnan R., Li Q. et al. RAGE modulates hypoxia/reoxygenation injury in adult murine cardiomyocytes via JNK and GSK-3beta signaling pathways // PLoS One. – 2010. – Vol. 5(4). – P. e10092.</mixed-citation><mixed-citation xml:lang="en">Shang L., Ananthakrishnan R., Li Q. et al. RAGE modulates hypoxia/reoxygenation injury in adult murine cardiomyocytes via JNK and GSK-3beta signaling pathways // PLoS One. – 2010. – Vol. 5(4). – P. e10092.</mixed-citation></citation-alternatives></ref><ref id="cit60"><label>60</label><citation-alternatives><mixed-citation xml:lang="ru">Shao Z., Bhattacharya K., Hsich E. et al. c-Jun N-terminal kinases mediate reactivation of Akt and cardiomyocyte survival after hypoxic injury in vitro and in vivo // Circ. Res. – 2006. – Vol. 98(1). – P. 111–118.</mixed-citation><mixed-citation xml:lang="en">Shao Z., Bhattacharya K., Hsich E. et al. c-Jun N-terminal kinases mediate reactivation of Akt and cardiomyocyte survival after hypoxic injury in vitro and in vivo // Circ. Res. – 2006. – Vol. 98(1). – P. 111–118.</mixed-citation></citation-alternatives></ref><ref id="cit61"><label>61</label><citation-alternatives><mixed-citation xml:lang="ru">Shi S., Li Q.S., Li H. et al. Anti-apoptotic action of hydrogen sulfide is associated with early JNK inhibition // Cell Biol. Int. – 2009. – Vol. 33(10). – P. 1095–1101.</mixed-citation><mixed-citation xml:lang="en">Shi S., Li Q.S., Li H. et al. Anti-apoptotic action of hydrogen sulfide is associated with early JNK inhibition // Cell Biol. Int. – 2009. – Vol. 33(10). – P. 1095–1101.</mixed-citation></citation-alternatives></ref><ref id="cit62"><label>62</label><citation-alternatives><mixed-citation xml:lang="ru">Song Z.F., Ji X.P., Li X.X. et al. Inhibition of the activity of poly (ADP-ribose) polymerase reduces heart ischaemia/reperfusion injury via suppressing JNK-mediated AIF translocation // Cell Mol. Med. – 2008. – Vol. 12(4). – P. 1220–1228.</mixed-citation><mixed-citation xml:lang="en">Song Z.F., Ji X.P., Li X.X. et al. Inhibition of the activity of poly (ADP-ribose) polymerase reduces heart ischaemia/reperfusion injury via suppressing JNK-mediated AIF translocation // Cell Mol. Med. – 2008. – Vol. 12(4). – P. 1220–1228.</mixed-citation></citation-alternatives></ref><ref id="cit63"><label>63</label><citation-alternatives><mixed-citation xml:lang="ru">Sun L., Isaak C.K., Zhou Y. et al. Salidroside and tyrosol from Rhodiola protect H9c2 cells from ischemia/reperfusion induced-apoptosis // Life Sci. – 2012. – Vol. 91(5–6). – P. 151–158.</mixed-citation><mixed-citation xml:lang="en">Sun L., Isaak C.K., Zhou Y. et al. Salidroside and tyrosol from Rhodiola protect H9c2 cells from ischemia/reperfusion induced-apoptosis // Life Sci. – 2012. – Vol. 91(5–6). – P. 151–158.</mixed-citation></citation-alternatives></ref><ref id="cit64"><label>64</label><citation-alternatives><mixed-citation xml:lang="ru">Sun H.Y., Wang N.P., Halkos M. et al. Postconditioning attenuates cardiomyocyte apoptosis via inhibition of JNK and p38 mitogen-activated protein kinase signaling pathways // Apoptosis. – 2006. – Vol. 11(9). – P. 1583–1593.</mixed-citation><mixed-citation xml:lang="en">Sun H.Y., Wang N.P., Halkos M. et al. Postconditioning attenuates cardiomyocyte apoptosis via inhibition of JNK and p38 mitogen-activated protein kinase signaling pathways // Apoptosis. – 2006. – Vol. 11(9). – P. 1583–1593.</mixed-citation></citation-alternatives></ref><ref id="cit65"><label>65</label><citation-alternatives><mixed-citation xml:lang="ru">Talmor D., Applebaum A., Rudich A. et al. Activation of mitogen-activated protein kinases in human heart during cardiopulmonary bypass // Circ. Res. – 2000. – Vol. 86(9). – P. 1004–1007.</mixed-citation><mixed-citation xml:lang="en">Talmor D., Applebaum A., Rudich A. et al. Activation of mitogen-activated protein kinases in human heart during cardiopulmonary bypass // Circ. Res. – 2000. – Vol. 86(9). – P. 1004–1007.</mixed-citation></citation-alternatives></ref><ref id="cit66"><label>66</label><citation-alternatives><mixed-citation xml:lang="ru">Vassalli G., Milano G., Moccetti T. Role of Mitogen-Activated Protein Kinases in myocardial ischemia reperfusion injury during heart transplantation // J. Transplant. – 2012. – Vol. 2012. – P. 928954.</mixed-citation><mixed-citation xml:lang="en">Vassalli G., Milano G., Moccetti T. Role of Mitogen-Activated Protein Kinases in myocardial ischemia reperfusion injury during heart transplantation // J. Transplant. – 2012. – Vol. 2012. – P. 928954.</mixed-citation></citation-alternatives></ref><ref id="cit67"><label>67</label><citation-alternatives><mixed-citation xml:lang="ru">Waetzig V., Herdegen T. Context-specific inhibition of JNKs: overcoming the dilemma of protection and damage // Trends Pharmacol. Sci. – 2005. – Vol. 26(9). – P. 455–461.</mixed-citation><mixed-citation xml:lang="en">Waetzig V., Herdegen T. Context-specific inhibition of JNKs: overcoming the dilemma of protection and damage // Trends Pharmacol. Sci. – 2005. – Vol. 26(9). – P. 455–461.</mixed-citation></citation-alternatives></ref><ref id="cit68"><label>68</label><citation-alternatives><mixed-citation xml:lang="ru">Walshe C.M., Laffey J.G., Kevin L. et al. Sepsis protects the myocardium and other organs from subsequent ischaemic/reperfusion injury via a MAPK dependent mechanism // Intensive Care Med. Exp. – 2015. – Vol. 3(1). – P. 35.</mixed-citation><mixed-citation xml:lang="en">Walshe C.M., Laffey J.G., Kevin L. et al. Sepsis protects the myocardium and other organs from subsequent ischaemic/reperfusion injury via a MAPK dependent mechanism // Intensive Care Med. Exp. – 2015. – Vol. 3(1). – P. 35.</mixed-citation></citation-alternatives></ref><ref id="cit69"><label>69</label><citation-alternatives><mixed-citation xml:lang="ru">Wang Z., Huang H., He W. et al. Regulator of G-protein signaling 5 protects cardiomyocytes against apoptosis during in vitro cardiac ischemia-reperfusion in mice by inhibiting both JNK and P38 signaling pathways [Electronic resource] // Biochem. Biophys. Res. Commun. – 2016. – Vol. 473(2). – P. 551–557.</mixed-citation><mixed-citation xml:lang="en">Wang Z., Huang H., He W. et al. Regulator of G-protein signaling 5 protects cardiomyocytes against apoptosis during in vitro cardiac ischemia-reperfusion in mice by inhibiting both JNK and P38 signaling pathways [Electronic resource] // Biochem. Biophys. Res. Commun. – 2016. – Vol. 473(2). – P. 551–557.</mixed-citation></citation-alternatives></ref><ref id="cit70"><label>70</label><citation-alternatives><mixed-citation xml:lang="ru">Wang J., Yang L., Rezaie A.R. et al. Activated protein C protects against myocardial ischemic/reperfusion injury through AMP-activated protein kinase signaling // J. Thromb. Haemost. – 2011. – Vol. 9(7). – P. 1308–1317.</mixed-citation><mixed-citation xml:lang="en">Wang J., Yang L., Rezaie A.R. et al. Activated protein C protects against myocardial ischemic/reperfusion injury through AMP-activated protein kinase signaling // J. Thromb. Haemost. – 2011. – Vol. 9(7). – P. 1308–1317.</mixed-citation></citation-alternatives></ref><ref id="cit71"><label>71</label><citation-alternatives><mixed-citation xml:lang="ru">Wei J., Wang W., Chopra I. et al. C-Jun N-terminal kinase (JNK-1) confers protection against brief but not extended ischemia during acute myocardial infarction // J. Biol. Chem. – 2011. – Vol. 286(16). – P. 13995–14006.</mixed-citation><mixed-citation xml:lang="en">Wei J., Wang W., Chopra I. et al. C-Jun N-terminal kinase (JNK-1) confers protection against brief but not extended ischemia during acute myocardial infarction // J. Biol. Chem. – 2011. – Vol. 286(16). – P. 13995–14006.</mixed-citation></citation-alternatives></ref><ref id="cit72"><label>72</label><citation-alternatives><mixed-citation xml:lang="ru">Wei C., Zhao Y., Wang L. et al. H2S restores the cardioprotection from ischemic post-conditioning in isolated aged rat hearts // Cell Biol. Int. – 2015. – Vol. 39(10). – P. 1173–1176.</mixed-citation><mixed-citation xml:lang="en">Wei C., Zhao Y., Wang L. et al. H2S restores the cardioprotection from ischemic post-conditioning in isolated aged rat hearts // Cell Biol. Int. – 2015. – Vol. 39(10). – P. 1173–1176.</mixed-citation></citation-alternatives></ref><ref id="cit73"><label>73</label><citation-alternatives><mixed-citation xml:lang="ru">Wiltshire C., Gillespie D.A., May G.H. Sab (SH3BP5), a novel mitochondria-localized JNK interacting protein // Biochem. Soc. Trans. – 2004. – Vol. 32 (Pt. 6). – P. 1075–1077.</mixed-citation><mixed-citation xml:lang="en">Wiltshire C., Gillespie D.A., May G.H. Sab (SH3BP5), a novel mitochondria-localized JNK interacting protein // Biochem. Soc. Trans. – 2004. – Vol. 32 (Pt. 6). – P. 1075–1077.</mixed-citation></citation-alternatives></ref><ref id="cit74"><label>74</label><citation-alternatives><mixed-citation xml:lang="ru">Wu J., Li J., Zhang N. et al. Stem cell-based therapies in ischemic-heart diseases: a focus on aspects of microcirculation and inflammation // Basic Res. Cardiol. – 2011. – Vol. 106(3). – P. 317–324.</mixed-citation><mixed-citation xml:lang="en">Wu J., Li J., Zhang N. et al. Stem cell-based therapies in ischemic-heart diseases: a focus on aspects of microcirculation and inflammation // Basic Res. Cardiol. – 2011. – Vol. 106(3). – P. 317–324.</mixed-citation></citation-alternatives></ref><ref id="cit75"><label>75</label><citation-alternatives><mixed-citation xml:lang="ru">Xie P., Guo S., Fan Y. et al. Atrogin-1/MAFbx enhances simulated ischemia/reperfusion induced apoptosis in cardiomyocytes through degradation of MAPK phosphatase-1 and sustained JNK-activation // J. Biol. Chem. – 2009. – Vol. 284(9). – P. 5488–5496.</mixed-citation><mixed-citation xml:lang="en">Xie P., Guo S., Fan Y. et al. Atrogin-1/MAFbx enhances simulated ischemia/reperfusion induced apoptosis in cardiomyocytes through degradation of MAPK phosphatase-1 and sustained JNK-activation // J. Biol. Chem. – 2009. – Vol. 284(9). – P. 5488–5496.</mixed-citation></citation-alternatives></ref><ref id="cit76"><label>76</label><citation-alternatives><mixed-citation xml:lang="ru">Xu J., Qin X., Cai X. et al. Mitochondrial JNK activation triggers autophagy and apoptosis and aggravates myocardial injury-following ischemia/reperfusion // Biochim. Biophys. Acta. – 2015. – Vol. 1852(2). – P. 262–270.</mixed-citation><mixed-citation xml:lang="en">Xu J., Qin X., Cai X. et al. Mitochondrial JNK activation triggers autophagy and apoptosis and aggravates myocardial injury-following ischemia/reperfusion // Biochim. Biophys. Acta. – 2015. – Vol. 1852(2). – P. 262–270.</mixed-citation></citation-alternatives></ref><ref id="cit77"><label>77</label><citation-alternatives><mixed-citation xml:lang="ru">Xu T., Wu X., Chen Q. et al. The anti-apoptotic and cardioprotective effects of salvianolic acid A on rat cardiomyocytes following ischemia/reperfusion by DUSP-mediated regulation of the ERK1/2/JNK pathway // PLoS One. – 2014. – Vol. 9(7). – P. e102292.</mixed-citation><mixed-citation xml:lang="en">Xu T., Wu X., Chen Q. et al. The anti-apoptotic and cardioprotective effects of salvianolic acid A on rat cardiomyocytes following ischemia/reperfusion by DUSP-mediated regulation of the ERK1/2/JNK pathway // PLoS One. – 2014. – Vol. 9(7). – P. e102292.</mixed-citation></citation-alternatives></ref><ref id="cit78"><label>78</label><citation-alternatives><mixed-citation xml:lang="ru">Xu H., Yao Y., Su Z. et al. Endogenous HMGB1 contributes to ischemia reperfusion-induced myocardial apoptosis by potentiating the effect of TNF-alpha/JNK // Am. J. Physiol. Heart Circ. Physiol. – 2011. – Vol. 300(3). – P. H913–921.</mixed-citation><mixed-citation xml:lang="en">Xu H., Yao Y., Su Z. et al. Endogenous HMGB1 contributes to ischemia reperfusion-induced myocardial apoptosis by potentiating the effect of TNF-alpha/JNK // Am. J. Physiol. Heart Circ. Physiol. – 2011. – Vol. 300(3). – P. H913–921.</mixed-citation></citation-alternatives></ref><ref id="cit79"><label>79</label><citation-alternatives><mixed-citation xml:lang="ru">Yang L.M., Xiao Y.L., Ou Yang J.H. Inhibition of magnesium lithospermate B on the c-Jun N-terminal kinase 3 mRNA-expression in cardiomyocytes encountered ischemia/reperfusion injury // Acta Pharmacol. Sin. – 2003. – Vol. 38(7). – P. 487–491.</mixed-citation><mixed-citation xml:lang="en">Yang L.M., Xiao Y.L., Ou Yang J.H. Inhibition of magnesium lithospermate B on the c-Jun N-terminal kinase 3 mRNA-expression in cardiomyocytes encountered ischemia/reperfusion injury // Acta Pharmacol. Sin. – 2003. – Vol. 38(7). – P. 487–491.</mixed-citation></citation-alternatives></ref><ref id="cit80"><label>80</label><citation-alternatives><mixed-citation xml:lang="ru">Yin T., Sandhu G., Wolfgang C.D. et al. Tissue specific pattern of stress kinase activation in ischemic/reperfused heart and kidney // J. Biol. Chem. – 1997. – Vol. 272(32). – P. 19943–19950.</mixed-citation><mixed-citation xml:lang="en">Yin T., Sandhu G., Wolfgang C.D. et al. Tissue specific pattern of stress kinase activation in ischemic/reperfused heart and kidney // J. Biol. Chem. – 1997. – Vol. 272(32). – P. 19943–19950.</mixed-citation></citation-alternatives></ref><ref id="cit81"><label>81</label><citation-alternatives><mixed-citation xml:lang="ru">Yue T.L., Wang C., Gu J.L. et al. Inhibition of extracellular signal-regulated kinase enhances ischemia/reoxygenation induced apoptosis in cultured cardiac myocytes and exaggerates reperfusion injury in isolated perfused heart // Circ. Res. – 2000. – Vol. 86(6). – P. 692–699.</mixed-citation><mixed-citation xml:lang="en">Yue T.L., Wang C., Gu J.L. et al. Inhibition of extracellular signal-regulated kinase enhances ischemia/reoxygenation induced apoptosis in cultured cardiac myocytes and exaggerates reperfusion injury in isolated perfused heart // Circ. Res. – 2000. – Vol. 86(6). – P. 692–699.</mixed-citation></citation-alternatives></ref><ref id="cit82"><label>82</label><citation-alternatives><mixed-citation xml:lang="ru">Zaha V.G., Qi D., Su K.N. et al. AMPK is critical for mitochondrial function during reperfusion after myocardial ischemia // J. Mol. Cell. Cardiol. – 2016. – Vol. 91. – P. 104–113.</mixed-citation><mixed-citation xml:lang="en">Zaha V.G., Qi D., Su K.N. et al. AMPK is critical for mitochondrial function during reperfusion after myocardial ischemia // J. Mol. Cell. Cardiol. – 2016. – Vol. 91. – P. 104–113.</mixed-citation></citation-alternatives></ref><ref id="cit83"><label>83</label><citation-alternatives><mixed-citation xml:lang="ru">Zhang J., Li X.X., Bian H.J. et al. Inhibition of the activity of Rho-kinase reduces cardiomyocyte apoptosis in heart ischemia/reperfusion via suppressing JNK-mediated AIF translocation // Clin. Chim. Acta. – 2009. – Vol. 401(1–2). – P. 76–80.</mixed-citation><mixed-citation xml:lang="en">Zhang J., Li X.X., Bian H.J. et al. Inhibition of the activity of Rho-kinase reduces cardiomyocyte apoptosis in heart ischemia/reperfusion via suppressing JNK-mediated AIF translocation // Clin. Chim. Acta. – 2009. – Vol. 401(1–2). – P. 76–80.</mixed-citation></citation-alternatives></ref><ref id="cit84"><label>84</label><citation-alternatives><mixed-citation xml:lang="ru">Zhang G.M., Wang Y., Li T.D. et al. Change of JNK MAPK and its influence on cardiocyte apoptosis in ischemic postconditioning // J. Zhejiang Univ. – 2009. – Vol. 38(6). – P. 611–619.</mixed-citation><mixed-citation xml:lang="en">Zhang G.M., Wang Y., Li T.D. et al. Change of JNK MAPK and its influence on cardiocyte apoptosis in ischemic postconditioning // J. Zhejiang Univ. – 2009. – Vol. 38(6). – P. 611–619.</mixed-citation></citation-alternatives></ref><ref id="cit85"><label>85</label><citation-alternatives><mixed-citation xml:lang="ru">Zhang G.M., Wang Y., Li T.D. et al. Post conditioning with gradually increased reperfusion provides better cardioprotection in rats // World J. Emerg. Med. – 2014. – Vol. 5(2). – P. 128–134.</mixed-citation><mixed-citation xml:lang="en">Zhang G.M., Wang Y., Li T.D. et al. Post conditioning with gradually increased reperfusion provides better cardioprotection in rats // World J. Emerg. Med. – 2014. – Vol. 5(2). – P. 128–134.</mixed-citation></citation-alternatives></ref><ref id="cit86"><label>86</label><citation-alternatives><mixed-citation xml:lang="ru">Zinkel S., Gross A., Yang E. BCL2 family in DNA damage and cell cycle control // Cell Death Differ. – 2006. – Vol. 13(8). – P. 1351–1359.</mixed-citation><mixed-citation xml:lang="en">Zinkel S., Gross A., Yang E. BCL2 family in DNA damage and cell cycle control // Cell Death Differ. – 2006. – Vol. 13(8). – P. 1351–1359.</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
