<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.3 20210610//EN" "JATS-journalpublishing1-3.dtd">
<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">10.29001/2073-8552-2024-39-3-26-33</article-id><article-id custom-type="elpub" pub-id-type="custom">cardiotomsk-2420</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>Ангиотензин 1-7 – пептид, повышающий резистентность сердца к ишемии и реперфузии: нарративный обзор</article-title><trans-title-group xml:lang="en"><trans-title>Angiotensin 1-7 – a peptide that increases the resistance of the heart to ischemia and reperfusion: narrative review</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-1808-556X</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Мухомедзянов</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Mukhomedzyanov</surname><given-names>A. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Мухомедзянов Александр Валерьевич, канд. мед. наук, научный сотрудник, лаборатория экспериментальной кардиологии</p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Alexander V. Mukhomedzyanov, Cand. Sci. (Med.), Research Scientist, Laboratory of Experimental Cardiology</p><p>111a, Kievskaya str., Tomsk, 634012</p></bio><email xlink:type="simple">sasha_m91@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-1607-1482</contrib-id><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>Попов Сергей Валентинович, д-р мед. наук, академик РАН, директор </p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Sergey V. Popov, Dr. Sci. (Med.), Academician of the Russian Academy of Sciences, Director </p><p>111a, Kievskaya str., Tomsk, 634012</p></bio><email xlink:type="simple">press@cardio-tomsk.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-6020-1598</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Маслов</surname><given-names>Л. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Maslov</surname><given-names>L. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Маслов Леонид Николаевич, д-р мед. наук, профессор, заведующий лабораторией экспериментальной кардиологии</p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Leonid N. Maslov, Dr. Sci. (Med.), Professor, Head of the Laboratory of Experimental Cardiology</p><p>111a, Kievskaya str., Tomsk, 634012</p></bio><email xlink:type="simple">maslov@cardio-tomsk.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-2264-1928</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Нарыжная</surname><given-names>Н. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Naryzhnaya</surname><given-names>N. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Нарыжная Наталья Владимировна, д-р мед. наук, ведущий научный сотрудник, лаборатория экспериментальной кардиологии</p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Natalia V. Naryzhnaya, Dr. Sci. (Med.)., Leading Research Scientist, Laboratory of Experimental Cardiology</p><p>111a, Kievskaya str., Tomsk, 634012</p></bio><email xlink:type="simple">natalynar@yandex.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-4502-0836</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Сиротина</surname><given-names>М. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Sirotina</surname><given-names>M. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Сиротина Мария Александровна, аспирант, младший научный сотрудник, лаборатория экспериментальной кардиологии</p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Maria A. Sirotina, Junior Research Scientist, Laboratory of Experimental Cardiology</p><p>111a, Kievskaya str., Tomsk, 634012</p></bio><email xlink:type="simple">sirotina_maria@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-9603-822X</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Курбатов</surname><given-names>Б. К.</given-names></name><name name-style="western" xml:lang="en"><surname>Kurbatov</surname><given-names>B. K.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Курбатов Борис Константинович, младший научный сотрудник, лаборатория экспериментальной кардиологии</p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Boris K. Kurbatov, Junior Research Scientist, Laboratory of Experimental Cardiology</p><p>111a, Kievskaya str., Tomsk, 634012</p></bio><email xlink:type="simple">bobersanker@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-5890-071X</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Горбунов</surname><given-names>А. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Gorbunov</surname><given-names>A. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Горбунов Александр Сергеевич, канд. мед. наук, старший научный сотрудник, лаборатория экспериментальной кардиологии</p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Alexsandr S. Gorbunov, Cand. Sci. (Med), Senior Research Scientist, Laboratory of Experimental Cardiology</p><p>111a, Kievskaya str., Tomsk, 634012</p></bio><email xlink:type="simple">shura.gorbunov.1982@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-4300-5763</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Килин</surname><given-names>М.</given-names></name><name name-style="western" xml:lang="en"><surname>Kilin</surname><given-names>M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Килин Михаил, лаборант, лаборатория экспериментальной кардиологии</p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Mikhail Kilin, Laboratory Assistant, Laboratory of Experimental Cardiology</p><p>111a, Kievskaya str., Tomsk, 634012</p></bio><email xlink:type="simple">Kilin112233@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-6418-1643</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Кан</surname><given-names>А.</given-names></name><name name-style="western" xml:lang="en"><surname>Kan</surname><given-names>A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Кан Артур, студент</p><p>634050, Томск, Московский тракт, 2</p></bio><bio xml:lang="en"><p>Artur Kan, Student</p><p>2, Moskovsky trakt, Tomsk, 634050</p></bio><email xlink:type="simple">kan989817@gmail.com</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-4341-3844</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Крылатов</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Krylatov</surname><given-names>A. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Крылатов Андрей Владимирович, канд. мед. наук, лаборант-исследователь, лаборатория экспериментальной кардиологии</p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Andrey V. Krylatov, Cand. Sci. (Med), Research Assistant, Laboratory of Experimental Cardiology</p><p>111a, Kievskaya str., Tomsk, 634012</p></bio><email xlink:type="simple">krylatovav@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8939-2340</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Подоксенов</surname><given-names>Ю. К.</given-names></name><name name-style="western" xml:lang="en"><surname>Podoksenov</surname><given-names>Yu. K.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Подоксенов Юрий Кириллович, д-р мед. наук, ведущий научный сотрудник, отделение анестезиологии-реанимации</p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Yury K. Podoksenov, Dr. Sci. (Med.) Leading Research Scientist, Department of Cardiovascular Surgery</p><p>111a, Kievskaya str., Tomsk, 634012</p></bio><email xlink:type="simple">uk@cardio-tomsk.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8543-6027</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Степанов</surname><given-names>И. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Stepanov</surname><given-names>I. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Степанов Иван Вадимович, канд. мед. наук, заведующий патологоанатомическим отделением</p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Ivan V. Stepanov, Cand. Sci. (Med.), Head of the Department of Morbid Anatomy</p><p>111a, Kievskaya str., Tomsk, 634012</p></bio><email xlink:type="simple">ivst@cardio-tomsk.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Научно-исследовательский институт кардиологии, Томский национальный исследовательский медицинский центр Российской академии наук (НИИ кардиологии Томского НИМЦ)</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Cardiology Research Institute, Tomsk National Research Medical Center of the Russian Academy of Sciences (Cardiology Research Institute, Tomsk NRMC)</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Сибирский государственный медицинский университет Министерства здравоохранения Российской Федерации (СибГМУ Минздрава России)</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Siberian State Medical University of the Ministry of Health of the Russian Federation (SSMU)</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2024</year></pub-date><pub-date pub-type="epub"><day>30</day><month>09</month><year>2024</year></pub-date><volume>39</volume><issue>3</issue><fpage>26</fpage><lpage>33</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Мухомедзянов А.В., Попов С.В., Маслов Л.Н., Нарыжная Н.В., Сиротина М.А., Курбатов Б.К., Горбунов А.С., Килин М., Кан А., Крылатов А.В., Подоксенов Ю.К., Степанов И.В., 2024</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="ru">Мухомедзянов А.В., Попов С.В., Маслов Л.Н., Нарыжная Н.В., Сиротина М.А., Курбатов Б.К., Горбунов А.С., Килин М., Кан А., Крылатов А.В., Подоксенов Ю.К., Степанов И.В.</copyright-holder><copyright-holder xml:lang="en">Mukhomedzyanov A.V., Popov S.V., Maslov L.N., Naryzhnaya N.V., Sirotina M.A., Kurbatov B.K., Gorbunov A.S., Kilin M., Kan A., Krylatov A.V., Podoksenov Y.K., Stepanov I.V.</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/2420">https://www.sibjcem.ru/jour/article/view/2420</self-uri><abstract><p>Обоснование. Высокая смертность среди пациентов с острым инфарктом миокарда (ОИМ) является важной проблемой современной кардиологии. В последние годы не произошло существенного снижения уровня смертности от ОИМ. Лекарственные препараты, применяемые для лечения ОИМ, недостаточно эффективны, поэтому назрела необходимость в разработке принципиально новых лекарственных препаратов, способных существенно увеличить толерантность сердца к ишемии/реперфузии (И/Р). Прототипом подобных лекарственных препаратов мог бы стать пептид ангиотензин 1-7, который способен повышать толерантность сердца к И/Р за счет активации Mas-рецепторов в ткани миокарда. В формировании кардиопротекторного эффекта ангиотензина 1-7 принимают участие следующие ферменты: NO-синтаза, растворимая гуанилилциклаза, PI3-киназа, ERK1/2 киназа, Akt-киназа и, возможно, протеинкиназа G. Косвенные данные указывают на то, что гипотетическим конечным эффектором в кардиопротекторном действии ангиотензина 1-7 могут быть митохондриальные или сарколеммальные АТФ-чувствительные К+-каналы.</p><p>Целью данной статьи является подготовка обзора информации о роли ангиотензина 1-7 в повышении резистентности сердца к ишемии и реперфузии. Поиск литературы по данному вопросу осуществлялся в базе данных PubMed с использованием запросов “angiotensin 1-7 receptors”, “stress”, “angiotensin 1-7”, “mas receptor”, “cardioprotective effects of angiotensin 1-7”.</p></abstract><trans-abstract xml:lang="en"><sec><title>Background</title><p>Background. The high mortality rate among patients with acute myocardial infarction (AMI) is an important problem of modern cardiology. In recent years, there has not been a significant decrease in mortality in AMI. Drugs used to treat AMI are not effective enough, so there is a need to develop fundamentally new drugs that can significantly increase the heart’s tolerance to ischemia/reperfusion (I/R). Angiotensin 1-7 peptide, which can increase cardiac tolerance to I/R by activating Mas receptor in myocardial tissue, could become a prototype of such drugs. The following enzymes are involved in the formation of the cardioprotective effect of angiotensin 1-7: NO-synthase, soluble guanylyl cyclase, phosphoinositide 3-kinase, extracellular signal-regulated kinases-1/2, Akt kinase and, possibly, protein kinase G. Indirect data indicate that the hypothetical end effector in the cardioprotective impact of angiotensin 1-7 could be mitochondrial or sarcolemmal ATP-sensitive K+ channel.</p></sec><sec><title>Aim</title><p>Aim: To review 1-7 role in increasing the heart resistance to ischemia and reperfusion. The literature search was carried out in the PubMed database with queries “angiotensin 1-7 receptors”, “stress”, “angiotensin 1-7”, “mas receptor”, “cardioprotective effects of angiotensin 1-7”.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>сердце</kwd><kwd>ишемия</kwd><kwd>реперфузия</kwd><kwd>острый инфаркт миокарда</kwd><kwd>ангиотензин 1-7</kwd><kwd>киназы</kwd><kwd>NO-синтаза</kwd></kwd-group><kwd-group xml:lang="en"><kwd>heart</kwd><kwd>ischemia</kwd><kwd>reperfusion</kwd><kwd>acute myocardial infarction</kwd><kwd>angiotensin 1-7</kwd><kwd>kinases</kwd><kwd>NO-synthase</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Меерсон Ф.З. Стресс-лимитирующие системы и проблема профилактики аритмии. Кардиология. 1987;27(7):5–12.</mixed-citation><mixed-citation xml:lang="en">Meerson F.Z. Stress-limiting systems and the problem of protection against arrhythmias. Kardiologiia. 1987;27(7):5–12. (In Russ.).</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Nakano Y., Matoba T., Tokutome M., Funamoto D., Katsuki S., Ikeda G. et al. Nanoparticle-mediated delivery of irbesartan induces cardioprotection from myocardial ischemia-reperfusion injury by antagonizing monocyte-mediated inflammation. Sci. Rep. 2016;6:29601. DOI: 10.1038/srep29601.</mixed-citation><mixed-citation xml:lang="en">Nakano Y., Matoba T., Tokutome M., Funamoto D., Katsuki S., Ikeda G. et al. Nanoparticle-mediated delivery of irbesartan induces cardioprotection from myocardial ischemia-reperfusion injury by antagonizing monocyte-mediated inflammation. Sci. Rep. 2016;6:29601. DOI: 10.1038/srep29601.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Jugdutt B.I., Jelani A., Palaniyappan A., Idikio H., Uweira R.E., Menon V. et al. Aging-related early changes in markers of ventricular and matrix remodeling after reperfused ST-segment elevation myocardial infarction in the canine model: effect of early therapy with an angiotensin II type 1 receptor blocker. Circulation. 2010;122(4):341–351. DOI: 10.1161/CIRCULATIONAHA.110.948190.</mixed-citation><mixed-citation xml:lang="en">Jugdutt B.I., Jelani A., Palaniyappan A., Idikio H., Uweira R.E., Menon V. et al. Aging-related early changes in markers of ventricular and matrix remodeling after reperfused ST-segment elevation myocardial infarction in the canine model: effect of early therapy with an angiotensin II type 1 receptor blocker. Circulation. 2010;122(4):341–351. DOI: 10.1161/CIRCULATIONAHA.110.948190.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Andrä M., Russ M., Jauk S., Lamacie M., Lang I., Arnold R. et al. Antioxidant solution in combination with angiotensin-(1-7) provides myocardial protection in langendorff-perfused rat hearts. Oxid. Med. Cell. Longev. 2020;2020:2862631. DOI: 10.1155/2020/2862631.</mixed-citation><mixed-citation xml:lang="en">Andrä M., Russ M., Jauk S., Lamacie M., Lang I., Arnold R. et al. Antioxidant solution in combination with angiotensin-(1-7) provides myocardial protection in langendorff-perfused rat hearts. Oxid. Med. Cell. Longev. 2020;2020:2862631. DOI: 10.1155/2020/2862631.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Zhou G., Fan L., Li Z., Li J., Kou X., Xiao M et al. G protein-coupled receptor MAS1 induces an inhibitory effect on myocardial infarction-induced myocardial injury. Int. J. Biol. Macromol. 2022;207:72–80. DOI: 10.1016/j.ijbiomac.2022.02.163.</mixed-citation><mixed-citation xml:lang="en">Zhou G., Fan L., Li Z., Li J., Kou X., Xiao M et al. G protein-coupled receptor MAS1 induces an inhibitory effect on myocardial infarction-induced myocardial injury. Int. J. Biol. Macromol. 2022;207:72–80. DOI: 10.1016/j.ijbiomac.2022.02.163.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Sykora M., Kratky V., Kopkan L., Tribulova N., Szeiffova Bacova B. Anti-fibrotic potential of angiotensin (1-7) in hemodynamically overloaded rat heart. Int. J. Mol. Sci. 2023;24(4):3490. DOI: 10.3390/ijms24043490.</mixed-citation><mixed-citation xml:lang="en">Sykora M., Kratky V., Kopkan L., Tribulova N., Szeiffova Bacova B. Anti-fibrotic potential of angiotensin (1-7) in hemodynamically overloaded rat heart. Int. J. Mol. Sci. 2023;24(4):3490. DOI: 10.3390/ijms24043490.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Young D., Waitches G., Birchmeier C., Fasano O., Wigler M. Isolation and characterization of a new cellular oncogene encoding a protein with multiple potential transmembrane domains. Cell. 1986;45(5):711–719. DOI: 10.1016/0092-8674(86)90785-3.</mixed-citation><mixed-citation xml:lang="en">Young D., Waitches G., Birchmeier C., Fasano O., Wigler M. Isolation and characterization of a new cellular oncogene encoding a protein with multiple potential transmembrane domains. Cell. 1986;45(5):711–719. DOI: 10.1016/0092-8674(86)90785-3.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Young D., O’Neill K., Jessell T., Wigler M. Characterization of the rat mas oncogene and its high-level expression in the hippocampus and cerebral cortex of rat brain. Proc. Natl. Acad. Sci. USA. 1988;85(14):5339–5342. DOI: 10.1073/pnas.85.14.5339.</mixed-citation><mixed-citation xml:lang="en">Young D., O’Neill K., Jessell T., Wigler M. Characterization of the rat mas oncogene and its high-level expression in the hippocampus and cerebral cortex of rat brain. Proc. Natl. Acad. Sci. USA. 1988;85(14):5339–5342. DOI: 10.1073/pnas.85.14.5339.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Metzger R., Bader M., Ludwig T., Berberich C., Bunnemann B., Ganten D. Expression of the mouse and rat mas proto-oncogene in the brain and peripheral tissues. FEBS Lett. 1995;357(1):27–32. DOI: 10.1016/0014-5793(94)01292-9.</mixed-citation><mixed-citation xml:lang="en">Metzger R., Bader M., Ludwig T., Berberich C., Bunnemann B., Ganten D. Expression of the mouse and rat mas proto-oncogene in the brain and peripheral tissues. FEBS Lett. 1995;357(1):27–32. DOI: 10.1016/0014-5793(94)01292-9.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Soltan F., Esmaili Dahej M., Yadegari M., Moradi A., Hafizi Barjin Z., Safari F. Resveratrol confers protection against ischemia/reperfusion injury by increase of angiotensin (1-7) expression in a rat model of myocardial hypertrophy. J. Cardiovasc. Pharmacol. 2021;78(1):e55–e64. DOI: 10.1097/FJC.0000000000001035.</mixed-citation><mixed-citation xml:lang="en">Soltan F., Esmaili Dahej M., Yadegari M., Moradi A., Hafizi Barjin Z., Safari F. Resveratrol confers protection against ischemia/reperfusion injury by increase of angiotensin (1-7) expression in a rat model of myocardial hypertrophy. J. Cardiovasc. Pharmacol. 2021;78(1):e55–e64. DOI: 10.1097/FJC.0000000000001035.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Kostenis E., Milligan G., Christopoulos A., Sanchez-Ferrer C.F., Heringer-Walther S., Sexton P.M. et al. G-protein-coupled receptor Mas is a physiological antagonist of the angiotensin II type 1 receptor. Circulation. 2005;111(14):1806–1813. DOI: 10.1161/01.CIR.0000160867.23556.7D.</mixed-citation><mixed-citation xml:lang="en">Kostenis E., Milligan G., Christopoulos A., Sanchez-Ferrer C.F., Heringer-Walther S., Sexton P.M. et al. G-protein-coupled receptor Mas is a physiological antagonist of the angiotensin II type 1 receptor. Circulation. 2005;111(14):1806–1813. DOI: 10.1161/01.CIR.0000160867.23556.7D.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Dias-Peixoto M.F., Ferreira A.J., Almeida P.W., Braga V.B., Coutinho D.C., Melo D.S. et al. The cardiac expression of Mas receptor is responsive to different physiological and pathological stimuli. Peptides. 2012;35(2):196–201. DOI: 10.1016/j.peptides.2012.03.022.</mixed-citation><mixed-citation xml:lang="en">Dias-Peixoto M.F., Ferreira A.J., Almeida P.W., Braga V.B., Coutinho D.C., Melo D.S. et al. The cardiac expression of Mas receptor is responsive to different physiological and pathological stimuli. Peptides. 2012;35(2):196–201. DOI: 10.1016/j.peptides.2012.03.022.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Zhao W., Zhao T., Chen Y., Sun Y. Angiotensin 1-7 promotes cardiac angiogenesis following infarction. Curr. Vasc. Pharmacol. 2015;13(1):37– 42. DOI: 10.2174/15701611113119990006.</mixed-citation><mixed-citation xml:lang="en">Zhao W., Zhao T., Chen Y., Sun Y. Angiotensin 1-7 promotes cardiac angiogenesis following infarction. Curr. Vasc. Pharmacol. 2015;13(1):37– 42. DOI: 10.2174/15701611113119990006.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Xu H., An X., Tian J., Fu M., Wang Q., Li C. et al. Angiotensin-(1-7) protects against sepsis-associated left ventricular dysfunction induced by lipopolysaccharide. Peptides. 2021;144:170612. DOI: 10.1016/j.peptides.2021.170612.</mixed-citation><mixed-citation xml:lang="en">Xu H., An X., Tian J., Fu M., Wang Q., Li C. et al. Angiotensin-(1-7) protects against sepsis-associated left ventricular dysfunction induced by lipopolysaccharide. Peptides. 2021;144:170612. DOI: 10.1016/j.peptides.2021.170612.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Tonnaer J.A., Engels G.M., Wiegant V.M., Burbach J.P., De Jong W., De Wied D. Proteolytic conversion of angiotensins in rat brain tissue. Eur. J. Biochem. 1983;131(2):415–421. DOI: 10.1111/j.1432-1033.1983.tb07279.x.</mixed-citation><mixed-citation xml:lang="en">Tonnaer J.A., Engels G.M., Wiegant V.M., Burbach J.P., De Jong W., De Wied D. Proteolytic conversion of angiotensins in rat brain tissue. Eur. J. Biochem. 1983;131(2):415–421. DOI: 10.1111/j.1432-1033.1983.tb07279.x.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Yu B., Chen H., Guo X.Q., Hua H., Guan Y., Cui F. et al. CIHH protects the heart against left ventricular remodelling and myocardial fibrosis by balancing the renin-angiotensin system in SHR. Life Sci. 2021;278:119540. DOI: 10.1016/j.lfs.2021.119540.</mixed-citation><mixed-citation xml:lang="en">Yu B., Chen H., Guo X.Q., Hua H., Guan Y., Cui F. et al. CIHH protects the heart against left ventricular remodelling and myocardial fibrosis by balancing the renin-angiotensin system in SHR. Life Sci. 2021;278:119540. DOI: 10.1016/j.lfs.2021.119540.</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">de Miranda D.C., de Oliveira Faria G., Hermidorff M.M., Dos Santos Silva F.C., de Assis L.V.M., Isoldi M.C. Pre- and post-conditioning of the heart: an overview of cardioprotective signaling pathways. Curr. Vasc. Pharmacol. 2021;19(5):499–524. DOI: 10.2174/1570161119666201120160619.</mixed-citation><mixed-citation xml:lang="en">de Miranda D.C., de Oliveira Faria G., Hermidorff M.M., Dos Santos Silva F.C., de Assis L.V.M., Isoldi M.C. Pre- and post-conditioning of the heart: an overview of cardioprotective signaling pathways. Curr. Vasc. Pharmacol. 2021;19(5):499–524. DOI: 10.2174/1570161119666201120160619.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Maslov L.N., Khaliulin I., Oeltgen P.R., Naryzhnaya N.V., Pei J.M., Brown S.A. et al. Prospects for creation of cardioprotective and antiarrhythmic drugs based on opioid receptor agonists. Med. Res. Rev. 2016a;36(5):871–923. DOI: 10.1002/med.21395.</mixed-citation><mixed-citation xml:lang="en">Maslov L.N., Khaliulin I., Oeltgen P.R., Naryzhnaya N.V., Pei J.M., Brown S.A. et al. Prospects for creation of cardioprotective and antiarrhythmic drugs based on opioid receptor agonists. Med. Res. Rev. 2016a;36(5):871–923. DOI: 10.1002/med.21395.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Maslov L.N., Khaliulin I., Zhang Y., Krylatov A.V., Naryzhnaya N.V., Mechoulam R. et al. Prospects for creation of cardioprotective drugs based on cannabinoid receptor agonists. J. Cardiovasc. Pharmacol. Ther. 2016;21(3):262–272. DOI: 10.1177/1074248415612593.</mixed-citation><mixed-citation xml:lang="en">Maslov L.N., Khaliulin I., Zhang Y., Krylatov A.V., Naryzhnaya N.V., Mechoulam R. et al. Prospects for creation of cardioprotective drugs based on cannabinoid receptor agonists. J. Cardiovasc. Pharmacol. Ther. 2016;21(3):262–272. DOI: 10.1177/1074248415612593.</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Canals M., Jenkins L., Kellett E., Milligan G. Up-regulation of the angiotensin II type 1 receptor by the MAS proto-oncogene is due to constitutive activation of Gq/G11 by MAS. J. Biol. Chem. 2006;281(24):16757– 16767. DOI: 10.1074/jbc.M601121200.</mixed-citation><mixed-citation xml:lang="en">Canals M., Jenkins L., Kellett E., Milligan G. Up-regulation of the angiotensin II type 1 receptor by the MAS proto-oncogene is due to constitutive activation of Gq/G11 by MAS. J. Biol. Chem. 2006;281(24):16757– 16767. DOI: 10.1074/jbc.M601121200.</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Sampaio W.O., Souza dos Santos R.A., Faria-Silva R., da Mata Machado L.T., Schiffrin E.L., Touyz R.M. Angiotensin-(1-7) through receptor Mas mediates endothelial nitric oxide synthase activation via Akt-dependent pathways. Hypertension. 2007;49(1):185–192. DOI: 10.1161/01.HYP.0000251865.35728.2f.</mixed-citation><mixed-citation xml:lang="en">Sampaio W.O., Souza dos Santos R.A., Faria-Silva R., da Mata Machado L.T., Schiffrin E.L., Touyz R.M. Angiotensin-(1-7) through receptor Mas mediates endothelial nitric oxide synthase activation via Akt-dependent pathways. Hypertension. 2007;49(1):185–192. DOI: 10.1161/01.HYP.0000251865.35728.2f.</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Lara L.D.S., Cavalcante F., Axelband F., De Souza A.M., Lopes A.G., Caruso-Neves C. Involvement of the Gi/o/cGMP/PKG pathway in the AT2-mediated inhibition of outer cortex proximal tubule Na+-ATPase by Ang-(1-7). Biochem. J. 2006;395(1):183–190. DOI: 10.1042/BJ20051455.</mixed-citation><mixed-citation xml:lang="en">Lara L.D.S., Cavalcante F., Axelband F., De Souza A.M., Lopes A.G., Caruso-Neves C. Involvement of the Gi/o/cGMP/PKG pathway in the AT2-mediated inhibition of outer cortex proximal tubule Na+-ATPase by Ang-(1-7). Biochem. J. 2006;395(1):183–190. DOI: 10.1042/BJ20051455.</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Teixeira L.B., Parreiras-E-Silva L.T., Bruder-Nascimento T., Duarte D.A., Simões S.C., Costa R.M. et al. Ang-(1-7) is an endogenous β-arrestin-biased agonist of the AT1 receptor with protective action in cardiac hypertrophy. Sci. Rep. 2017;7(1):11903. DOI: 10.1038/s41598-017-12074-3.</mixed-citation><mixed-citation xml:lang="en">Teixeira L.B., Parreiras-E-Silva L.T., Bruder-Nascimento T., Duarte D.A., Simões S.C., Costa R.M. et al. Ang-(1-7) is an endogenous β-arrestin-biased agonist of the AT1 receptor with protective action in cardiac hypertrophy. Sci. Rep. 2017;7(1):11903. DOI: 10.1038/s41598-017-12074-3.</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Galandrin S., Denis C., Boularan C., Marie J., M’Kadmi C., Pilette C. et al. Cardioprotective angiotensin-(1-7) peptide acts as a natural-biased ligand at the angiotensin II type 1 receptor. Hypertension. 2016;68(6):1365–1374. DOI: 10.1161/HYPERTENSIONAHA.116.08118.</mixed-citation><mixed-citation xml:lang="en">Galandrin S., Denis C., Boularan C., Marie J., M’Kadmi C., Pilette C. et al. Cardioprotective angiotensin-(1-7) peptide acts as a natural-biased ligand at the angiotensin II type 1 receptor. Hypertension. 2016;68(6):1365–1374. DOI: 10.1161/HYPERTENSIONAHA.116.08118.</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Oudot A., Vergely C., Ecarnot-Laubriet A., Rochette L. Pharmacological concentration of angiotensin-(1-7) activates NADPH oxidase after ischemia-reperfusion in rat heart through AT1 receptor stimulation. Regul. Pept. 2005;127(1–3):101–110. DOI: 10.1016/j.regpep.2004.10.013.</mixed-citation><mixed-citation xml:lang="en">Oudot A., Vergely C., Ecarnot-Laubriet A., Rochette L. Pharmacological concentration of angiotensin-(1-7) activates NADPH oxidase after ischemia-reperfusion in rat heart through AT1 receptor stimulation. Regul. Pept. 2005;127(1–3):101–110. DOI: 10.1016/j.regpep.2004.10.013.</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Gaidarov I., Adams J., Frazer J., Anthony T., Chen X., Gatlin J. et al. Angiotensin (1-7) does not interact directly with MAS1, but can potently antagonize signaling from the AT1 receptor. Cell. Signal. 2018;50:9–24. DOI: 10.1016/j.cellsig.2018.06.007.</mixed-citation><mixed-citation xml:lang="en">Gaidarov I., Adams J., Frazer J., Anthony T., Chen X., Gatlin J. et al. Angiotensin (1-7) does not interact directly with MAS1, but can potently antagonize signaling from the AT1 receptor. Cell. Signal. 2018;50:9–24. DOI: 10.1016/j.cellsig.2018.06.007.</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Ferreira A.J., Santos R.A., Almeida A.P. Angiotensin-(1-7): cardioprotective effect in myocardial ischemia/reperfusion. Hypertension. 2001;38(3 Pt.2):665–668. DOI: 10.1161/01.hyp.38.3.665.</mixed-citation><mixed-citation xml:lang="en">Ferreira A.J., Santos R.A., Almeida A.P. Angiotensin-(1-7): cardioprotective effect in myocardial ischemia/reperfusion. Hypertension. 2001;38(3 Pt.2):665–668. DOI: 10.1161/01.hyp.38.3.665.</mixed-citation></citation-alternatives></ref><ref id="cit28"><label>28</label><citation-alternatives><mixed-citation xml:lang="ru">Savergnini S.Q., Beiman M., Lautner R.Q., de Paula-Carvalho V., Allahdadi K., Pessoa D.C. et al. Vascular relaxation, antihypertensive effect, and cardioprotection of a novel peptide agonist of the MAS receptor. Hypertension. 2010;56(1):112–120. DOI: 10.1161/HYPERTENSIONAHA.110.152942.</mixed-citation><mixed-citation xml:lang="en">Savergnini S.Q., Beiman M., Lautner R.Q., de Paula-Carvalho V., Allahdadi K., Pessoa D.C. et al. Vascular relaxation, antihypertensive effect, and cardioprotection of a novel peptide agonist of the MAS receptor. Hypertension. 2010;56(1):112–120. DOI: 10.1161/HYPERTENSIONAHA.110.152942.</mixed-citation></citation-alternatives></ref><ref id="cit29"><label>29</label><citation-alternatives><mixed-citation xml:lang="ru">Ferreira A.J., Santos R.A., Almeida A.P. Angiotensin-(1-7) improves the post-ischemic function in isolated perfused rat hearts. Braz. J. Med. Biol. Res. 2002;35(9):1083–1090. DOI: 10.1590/s0100-879x2002000900009.</mixed-citation><mixed-citation xml:lang="en">Ferreira A.J., Santos R.A., Almeida A.P. Angiotensin-(1-7) improves the post-ischemic function in isolated perfused rat hearts. Braz. J. Med. Biol. Res. 2002;35(9):1083–1090. DOI: 10.1590/s0100-879x2002000900009.</mixed-citation></citation-alternatives></ref><ref id="cit30"><label>30</label><citation-alternatives><mixed-citation xml:lang="ru">Castro C.H., Santos R.A., Ferreira A.J., Bader M., Alenina N., Almeida A.P. Effects of genetic deletion of angiotensin-(1-7) receptor Mas on cardiac function during ischemia/reperfusion in the isolated perfused mouse heart. Life Sci. 2006;80(3):264–268. DOI: 10.1016/j.lfs.2006.09.007.</mixed-citation><mixed-citation xml:lang="en">Castro C.H., Santos R.A., Ferreira A.J., Bader M., Alenina N., Almeida A.P. Effects of genetic deletion of angiotensin-(1-7) receptor Mas on cardiac function during ischemia/reperfusion in the isolated perfused mouse heart. Life Sci. 2006;80(3):264–268. DOI: 10.1016/j.lfs.2006.09.007.</mixed-citation></citation-alternatives></ref><ref id="cit31"><label>31</label><citation-alternatives><mixed-citation xml:lang="ru">Liao X.X., Guo R.X., Ma H., Wang L.C., Chen Z.H., Yang C.T. et al. Effects of angiotensin-(1-7) on oxidative stress and functional changes of isolated rat hearts induced by ischemia-reperfusion. Nan Fang Yi Ke Da Xue Xue Bao. 2008;28(8):1345–1348. [In Chinese].</mixed-citation><mixed-citation xml:lang="en">Liao X.X., Guo R.X., Ma H., Wang L.C., Chen Z.H., Yang C.T. et al. Effects of angiotensin-(1-7) on oxidative stress and functional changes of isolated rat hearts induced by ischemia-reperfusion. Nan Fang Yi Ke Da Xue Xue Bao. 2008;28(8):1345–1348. [In Chinese].</mixed-citation></citation-alternatives></ref><ref id="cit32"><label>32</label><citation-alternatives><mixed-citation xml:lang="ru">Al-Maghrebi M., Benter I.F., Diz D.I. Endogenous angiotensin-(1-7) reduces cardiac ischemia-induced dysfunction in diabetic hypertensive rats. Pharmacol. Res. 2009;59(4):263–268. DOI: 10.1016/j.phrs.2008.12.008.</mixed-citation><mixed-citation xml:lang="en">Al-Maghrebi M., Benter I.F., Diz D.I. Endogenous angiotensin-(1-7) reduces cardiac ischemia-induced dysfunction in diabetic hypertensive rats. Pharmacol. Res. 2009;59(4):263–268. DOI: 10.1016/j.phrs.2008.12.008.</mixed-citation></citation-alternatives></ref><ref id="cit33"><label>33</label><citation-alternatives><mixed-citation xml:lang="ru">Marques F.D., Ferreira A.J., Sinisterra R.D., Jacoby B.A., Sousa F.B., Caliari M.V. et al. An oral formulation of angiotensin-(1-7) produces cardioprotective effects in infarcted and isoproterenol-treated rats. Hypertension. 2011;57(3):477–483. DOI: 10.1161/HYPERTENSIONAHA.110.167346.</mixed-citation><mixed-citation xml:lang="en">Marques F.D., Ferreira A.J., Sinisterra R.D., Jacoby B.A., Sousa F.B., Caliari M.V. et al. An oral formulation of angiotensin-(1-7) produces cardioprotective effects in infarcted and isoproterenol-treated rats. Hypertension. 2011;57(3):477–483. DOI: 10.1161/HYPERTENSIONAHA.110.167346.</mixed-citation></citation-alternatives></ref><ref id="cit34"><label>34</label><citation-alternatives><mixed-citation xml:lang="ru">Maslov L.N., Popov S.V., Mukhomedzyanov A.V., Naryzhnaya N.V., Voronkov N.S., Ryabov V.V. et al. Reperfusion cardiac injury: Receptors and the signaling mechanisms. Curr. Cardiol. Rev. 2022;18(5):63–79. DOI: 10.2174/1573403X18666220413121730.</mixed-citation><mixed-citation xml:lang="en">Maslov L.N., Popov S.V., Mukhomedzyanov A.V., Naryzhnaya N.V., Voronkov N.S., Ryabov V.V. et al. Reperfusion cardiac injury: Receptors and the signaling mechanisms. Curr. Cardiol. Rev. 2022;18(5):63–79. DOI: 10.2174/1573403X18666220413121730.</mixed-citation></citation-alternatives></ref><ref id="cit35"><label>35</label><citation-alternatives><mixed-citation xml:lang="ru">Liao X., Wang L., Yang C., He J., Wang X., Guo R. et al. Cyclooxygenase mediates cardioprotection of angiotensin-(1-7) against ischemia/ reperfusion-induced injury through the inhibition of oxidative stress. Mol. Med. Rep. 2011;4(6):1145–1150. DOI: 10.3892/mmr.2011.570.</mixed-citation><mixed-citation xml:lang="en">Liao X., Wang L., Yang C., He J., Wang X., Guo R. et al. Cyclooxygenase mediates cardioprotection of angiotensin-(1-7) against ischemia/ reperfusion-induced injury through the inhibition of oxidative stress. Mol. Med. Rep. 2011;4(6):1145–1150. DOI: 10.3892/mmr.2011.570.</mixed-citation></citation-alternatives></ref><ref id="cit36"><label>36</label><citation-alternatives><mixed-citation xml:lang="ru">Wang L., Luo D., Liao X., He J., Liu C., Yang C. et al. Ang-(1-7) offers cytoprotection against ischemia-reperfusion injury by restoring intracellular calcium homeostasis. J. Cardiovasc. Pharmacol. 2014;63(3):259–264. DOI: 10.1097/FJC.0000000000000043.</mixed-citation><mixed-citation xml:lang="en">Wang L., Luo D., Liao X., He J., Liu C., Yang C. et al. Ang-(1-7) offers cytoprotection against ischemia-reperfusion injury by restoring intracellular calcium homeostasis. J. Cardiovasc. Pharmacol. 2014;63(3):259–264. DOI: 10.1097/FJC.0000000000000043.</mixed-citation></citation-alternatives></ref><ref id="cit37"><label>37</label><citation-alternatives><mixed-citation xml:lang="ru">Zhao P., Li F., Gao W., Wang J., Fu L., Chen Y. et al. Angiotensin1-7 protects cardiomyocytes from hypoxia/reoxygenation-induced oxidative stress by preventing ROS-associated mitochondrial dysfunction and activating the Akt signaling pathway. Acta Histochem. 2015;117(8):803– 810. DOI: 10.1016/j.acthis.2015.07.004.</mixed-citation><mixed-citation xml:lang="en">Zhao P., Li F., Gao W., Wang J., Fu L., Chen Y. et al. Angiotensin1-7 protects cardiomyocytes from hypoxia/reoxygenation-induced oxidative stress by preventing ROS-associated mitochondrial dysfunction and activating the Akt signaling pathway. Acta Histochem. 2015;117(8):803– 810. DOI: 10.1016/j.acthis.2015.07.004.</mixed-citation></citation-alternatives></ref><ref id="cit38"><label>38</label><citation-alternatives><mixed-citation xml:lang="ru">Abwainy A., Babiker F., Akhtar S., Benter I.F. Endogenous angiotensin-(1-7)/Mas receptor/NO pathway mediates the cardioprotective effects of pacing postconditioning. Am. J. Physiol. Heart Circ. Physiol. 2016;310(1):H104–H112. DOI: 10.1152/ajpheart.00121.2015.</mixed-citation><mixed-citation xml:lang="en">Abwainy A., Babiker F., Akhtar S., Benter I.F. Endogenous angiotensin-(1-7)/Mas receptor/NO pathway mediates the cardioprotective effects of pacing postconditioning. Am. J. Physiol. Heart Circ. Physiol. 2016;310(1):H104–H112. DOI: 10.1152/ajpheart.00121.2015.</mixed-citation></citation-alternatives></ref><ref id="cit39"><label>39</label><citation-alternatives><mixed-citation xml:lang="ru">Akhtar S., Babiker F., Akhtar U.A., Benter I.F. mitigating cardiotoxicity of dendrimers: angiotensin-(1-7) via its mas receptor ameliorates PAMAM-induced cardiac dysfunction in the isolated mammalian heart. Pharmaceutics. 2022;14(12):2673. DOI: 10.3390/pharmaceutics14122673.</mixed-citation><mixed-citation xml:lang="en">Akhtar S., Babiker F., Akhtar U.A., Benter I.F. mitigating cardiotoxicity of dendrimers: angiotensin-(1-7) via its mas receptor ameliorates PAMAM-induced cardiac dysfunction in the isolated mammalian heart. Pharmaceutics. 2022;14(12):2673. DOI: 10.3390/pharmaceutics14122673.</mixed-citation></citation-alternatives></ref><ref id="cit40"><label>40</label><citation-alternatives><mixed-citation xml:lang="ru">Brosnihan K.B., Li P., Ferrario C.M. Angiotensin-(1-7) dilates canine coronary arteries through kinins and nitric oxide. Hypertension. 1996;27(3 Pt.2):523–528. DOI: 10.1161/01.hyp.27.3.523.</mixed-citation><mixed-citation xml:lang="en">Brosnihan K.B., Li P., Ferrario C.M. Angiotensin-(1-7) dilates canine coronary arteries through kinins and nitric oxide. Hypertension. 1996;27(3 Pt.2):523–528. DOI: 10.1161/01.hyp.27.3.523.</mixed-citation></citation-alternatives></ref><ref id="cit41"><label>41</label><citation-alternatives><mixed-citation xml:lang="ru">Heitsch H., Brovkovych S., Malinski T., Wiemer G. Angiotensin-(1-7)-stimulated nitric oxide and superoxide release from endothelial cells. Hypertension. 2001;37(1):72–76. DOI: 10.1161/01.hyp.37.1.72.</mixed-citation><mixed-citation xml:lang="en">Heitsch H., Brovkovych S., Malinski T., Wiemer G. Angiotensin-(1-7)-stimulated nitric oxide and superoxide release from endothelial cells. Hypertension. 2001;37(1):72–76. DOI: 10.1161/01.hyp.37.1.72.</mixed-citation></citation-alternatives></ref><ref id="cit42"><label>42</label><citation-alternatives><mixed-citation xml:lang="ru">Dias-Peixoto M.F., Santos R.A., Gomes E.R., Alves M.N., Almeida P.W., Greco L. et al. Molecular mechanisms involved in the angiotensin-(1-7)/Mas signaling pathway in cardiomyocytes. Hypertension. 2008;52(3):542–548. DOI: 10.1161/HYPERTENSIONAHA.108.114280.</mixed-citation><mixed-citation xml:lang="en">Dias-Peixoto M.F., Santos R.A., Gomes E.R., Alves M.N., Almeida P.W., Greco L. et al. Molecular mechanisms involved in the angiotensin-(1-7)/Mas signaling pathway in cardiomyocytes. Hypertension. 2008;52(3):542–548. DOI: 10.1161/HYPERTENSIONAHA.108.114280.</mixed-citation></citation-alternatives></ref><ref id="cit43"><label>43</label><citation-alternatives><mixed-citation xml:lang="ru">de Almeida P.W., de Freitas Lima R., de Morais Gomes E.R., Rocha-Resende C., Roman-Campos D., Gondim A.N. et al. Functional cross-talk between aldosterone and angiotensin-(1-7) in ventricular myocytes. Hypertension. 2013;61(2):425–430. DOI: 10.1161/HYPERTENSIONAHA.111.199539.</mixed-citation><mixed-citation xml:lang="en">de Almeida P.W., de Freitas Lima R., de Morais Gomes E.R., Rocha-Resende C., Roman-Campos D., Gondim A.N. et al. Functional cross-talk between aldosterone and angiotensin-(1-7) in ventricular myocytes. Hypertension. 2013;61(2):425–430. DOI: 10.1161/HYPERTENSIONAHA.111.199539.</mixed-citation></citation-alternatives></ref><ref id="cit44"><label>44</label><citation-alternatives><mixed-citation xml:lang="ru">Gomes E.R., Lara A.A., Almeida P.W., Guimarães D., Resende R.R., Campagnole-Santos M.J. et al. Angiotensin-(1-7) prevents cardiomyocyte pathological remodeling through a nitric oxide/guanosine 3’,5’-cyclic monophosphate-dependent pathway. Hypertension. 2010;55(1):153– 60. DOI: 10.1161/HYPERTENSIONAHA.109.143255.</mixed-citation><mixed-citation xml:lang="en">Gomes E.R., Lara A.A., Almeida P.W., Guimarães D., Resende R.R., Campagnole-Santos M.J. et al. Angiotensin-(1-7) prevents cardiomyocyte pathological remodeling through a nitric oxide/guanosine 3’,5’-cyclic monophosphate-dependent pathway. Hypertension. 2010;55(1):153– 60. DOI: 10.1161/HYPERTENSIONAHA.109.143255.</mixed-citation></citation-alternatives></ref><ref id="cit45"><label>45</label><citation-alternatives><mixed-citation xml:lang="ru">Zhu L., Liu Z., Huang L.P., Zhou H.R., Cao Y., Yang X.P. et al. Angiotensin (1-7) alleviates postresuscitation myocardial dysfunction by suppressing oxidative stress through the phosphoinositide 3-kinase, protein kinase B, and endothelial nitric oxide synthase signaling pathway. J. Cardiovasc. Pharmacol. 2021;78(1):e65–e76. DOI: 10.1097/FJC.0000000000001037.</mixed-citation><mixed-citation xml:lang="en">Zhu L., Liu Z., Huang L.P., Zhou H.R., Cao Y., Yang X.P. et al. Angiotensin (1-7) alleviates postresuscitation myocardial dysfunction by suppressing oxidative stress through the phosphoinositide 3-kinase, protein kinase B, and endothelial nitric oxide synthase signaling pathway. J. Cardiovasc. Pharmacol. 2021;78(1):e65–e76. DOI: 10.1097/FJC.0000000000001037.</mixed-citation></citation-alternatives></ref><ref id="cit46"><label>46</label><citation-alternatives><mixed-citation xml:lang="ru">Giani J.F., Gironacci M.M., Muñoz M.C., Peña C., Turyn D., Dominici F.P. Angiotensin-(1 7) stimulates the phosphorylation of JAK2, IRS-1 and Akt in rat heart in vivo: role of the AT1 and Mas receptors. Am. J. Physiol. Heart Circ. Physiol. 2007;293(2):H1154–H1163. DOI: 10.1152/ajpheart.01395.2006.</mixed-citation><mixed-citation xml:lang="en">Giani J.F., Gironacci M.M., Muñoz M.C., Peña C., Turyn D., Dominici F.P. Angiotensin-(1 7) stimulates the phosphorylation of JAK2, IRS-1 and Akt in rat heart in vivo: role of the AT1 and Mas receptors. Am. J. Physiol. Heart Circ. Physiol. 2007;293(2):H1154–H1163. DOI: 10.1152/ajpheart.01395.2006.</mixed-citation></citation-alternatives></ref><ref id="cit47"><label>47</label><citation-alternatives><mixed-citation xml:lang="ru">Giani J.F., Gironacci M.M., Muñoz M.C., Turyn D., Dominici F.P. Angiotensin-(1-7) has a dual role on growth-promoting signaling pathways in rat heart in vivo by stimulating STAT3 and STAT5a/b phosphorylation and inhibiting angiotensin II-stimulated ERK1/2 and Rho kinase activity. Exp. Physiol. 2008;93(5):570–578. DOI: 10.1113/expphysiol.2007.014269.</mixed-citation><mixed-citation xml:lang="en">Giani J.F., Gironacci M.M., Muñoz M.C., Turyn D., Dominici F.P. Angiotensin-(1-7) has a dual role on growth-promoting signaling pathways in rat heart in vivo by stimulating STAT3 and STAT5a/b phosphorylation and inhibiting angiotensin II-stimulated ERK1/2 and Rho kinase activity. Exp. Physiol. 2008;93(5):570–578. DOI: 10.1113/expphysiol.2007.014269.</mixed-citation></citation-alternatives></ref><ref id="cit48"><label>48</label><citation-alternatives><mixed-citation xml:lang="ru">Zhao J., Liu E., Li G., Qi L., Li J., Yang W. Effects of the angiotensin-(1-7)/Mas/PI3K/Akt/nitric oxide axis and the possible role of atrial natriuretic peptide in an acute atrial tachycardia canine model. J. Renin Angiotensin Aldosterone Syst. 2015;16(4):1069–1077. DOI: 10.1177/1470320314543723.</mixed-citation><mixed-citation xml:lang="en">Zhao J., Liu E., Li G., Qi L., Li J., Yang W. Effects of the angiotensin-(1-7)/Mas/PI3K/Akt/nitric oxide axis and the possible role of atrial natriuretic peptide in an acute atrial tachycardia canine model. J. Renin Angiotensin Aldosterone Syst. 2015;16(4):1069–1077. DOI: 10.1177/1470320314543723.</mixed-citation></citation-alternatives></ref><ref id="cit49"><label>49</label><citation-alternatives><mixed-citation xml:lang="ru">Lei Y., Xu Q., Zeng B., Zhang W., Zhen Y., Zhai Y. et al. Angiotensin-(1-7) protects cardiomyocytes against high glucose-induced injuries through inhibiting reactive oxygen species-activated leptin-p38 mitogen-activated protein kinase/extracellular signal-regulated protein kinase 1/2 pathways, but not the leptin-c-Jun N-terminal kinase pathway in vitro. J. Diabetes Investig. 2017;8(4):434–445. DOI: 10.1111/jdi.12603.</mixed-citation><mixed-citation xml:lang="en">Lei Y., Xu Q., Zeng B., Zhang W., Zhen Y., Zhai Y. et al. Angiotensin-(1-7) protects cardiomyocytes against high glucose-induced injuries through inhibiting reactive oxygen species-activated leptin-p38 mitogen-activated protein kinase/extracellular signal-regulated protein kinase 1/2 pathways, but not the leptin-c-Jun N-terminal kinase pathway in vitro. J. Diabetes Investig. 2017;8(4):434–445. DOI: 10.1111/jdi.12603.</mixed-citation></citation-alternatives></ref><ref id="cit50"><label>50</label><citation-alternatives><mixed-citation xml:lang="ru">Cerniello F.M., Carretero O.A., Longo Carbajosa N.A., Cerrato B.D., Santos R.A., Grecco H.E. et al. MAS1 receptor trafficking Involves ERK1/2 activation through a β-Arrestin2-dependent pathway. Hypertension. 2017;70(5):982–989. DOI: 10.1161/HYPERTENSIONAHA.117.09789.</mixed-citation><mixed-citation xml:lang="en">Cerniello F.M., Carretero O.A., Longo Carbajosa N.A., Cerrato B.D., Santos R.A., Grecco H.E. et al. MAS1 receptor trafficking Involves ERK1/2 activation through a β-Arrestin2-dependent pathway. Hypertension. 2017;70(5):982–989. DOI: 10.1161/HYPERTENSIONAHA.117.09789.</mixed-citation></citation-alternatives></ref><ref id="cit51"><label>51</label><citation-alternatives><mixed-citation xml:lang="ru">Lu Y.Y., Wu W.S., Lin Y.K., Cheng C.C., Chen Y.C., Chen S.A. et al. Angiotensin 1-7 modulates electrophysiological characteristics and calcium homoeostasis in pulmonary veins cardiomyocytes via MAS/PI3K/ eNOS signalling pathway. Eur. J. Clin. Invest. 2018;48(1):e12854. DOI: 10.1111/eci.12854.</mixed-citation><mixed-citation xml:lang="en">Lu Y.Y., Wu W.S., Lin Y.K., Cheng C.C., Chen Y.C., Chen S.A. et al. Angiotensin 1-7 modulates electrophysiological characteristics and calcium homoeostasis in pulmonary veins cardiomyocytes via MAS/PI3K/ eNOS signalling pathway. Eur. J. Clin. Invest. 2018;48(1):e12854. DOI: 10.1111/eci.12854.</mixed-citation></citation-alternatives></ref><ref id="cit52"><label>52</label><citation-alternatives><mixed-citation xml:lang="ru">Yang Y.Y., Sun X.T., Li Z.X., Chen W.Y., Wang X., Liang M.L. et al. Protective effect of angiotensin-(1-7) against hyperglycaemia-induced injury in H9c2 cardiomyoblast cells via the PI3K̸Akt signaling pathway. Int. J. Mol. Med. 2018;41(3):1283–1292. DOI: 10.3892/ijmm.2017.3322.</mixed-citation><mixed-citation xml:lang="en">Yang Y.Y., Sun X.T., Li Z.X., Chen W.Y., Wang X., Liang M.L. et al. Protective effect of angiotensin-(1-7) against hyperglycaemia-induced injury in H9c2 cardiomyoblast cells via the PI3K̸Akt signaling pathway. Int. J. Mol. Med. 2018;41(3):1283–1292. DOI: 10.3892/ijmm.2017.3322.</mixed-citation></citation-alternatives></ref><ref id="cit53"><label>53</label><citation-alternatives><mixed-citation xml:lang="ru">Costa A., Galdino G., Romero T., Silva G., Cortes S., Santos R. et al. Ang- (1-7) activates the NO/cGMP and ATP-sensitive K+ channels pathway to induce peripheral antinociception in rats. Nitric. Oxide. 2014;37:11–16. DOI: 10.1016/j.niox.2013.12.007.</mixed-citation><mixed-citation xml:lang="en">Costa A., Galdino G., Romero T., Silva G., Cortes S., Santos R. et al. Ang- (1-7) activates the NO/cGMP and ATP-sensitive K+ channels pathway to induce peripheral antinociception in rats. Nitric. Oxide. 2014;37:11–16. DOI: 10.1016/j.niox.2013.12.007.</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>
