<?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">10.29001/2073-8552-2025-40-4-123-130</article-id><article-id custom-type="elpub" pub-id-type="custom">cardiotomsk-2917</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>КЛИНИЧЕСКИЕ ИССЛЕДОВАНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>CLINICAL STUDIES</subject></subj-group></article-categories><title-group><article-title>Ассоциация полиморфизмов C7028T, G3010A, G9055A митохондриальной ДНК и тяжести течения хронической сердечной недостаточности ишемического генеза</article-title><trans-title-group xml:lang="en"><trans-title>Association of mitochondrial DNA C7028T, G3010A, G9055A polymorphisms and the severity of chronic heart failure of ischemic genesis</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-7361-2161</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Муслимова</surname><given-names>Э. Ф.</given-names></name><name name-style="western" xml:lang="en"><surname>Muslimova</surname><given-names>E. F.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Муслимова Эльвира Фаритовна - канд. мед. наук, научный сотрудник, лаборатория молекулярно-клеточной патологии и генодиагностики, НИИ кардиологии Томского НИМЦ.</p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Elvira F. Muslimova - Cand. Sci. (Med.), Research Scientist, Laboratory of Molecular and Cellular Pathology and Gene Diagnostics, Cardiology Research Institute, Tomsk NRMC.</p><p>634012, Tomsk, Kievskaya str., 111a</p></bio><email xlink:type="simple">muslimovef@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/0000-0002-8070-2234</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Кужелева</surname><given-names>Е. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Kuzheleva</surname><given-names>E. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Кужелева Елена Андреевна - канд. мед. наук, старший научный сотрудник, отделение патологии миокарда, НИИ кардиологии Томского НИМЦ.</p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Elena A. Kuzheleva - Cand. Sci. (Med.), Senior Research Scientist, Department of Myocardial Pathology, Cardiology Research Institute, Tomsk NRMC.</p><p>634012, Tomsk, Kievskaya str., 111a</p></bio><email xlink:type="simple">kea@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/0000-0002-9488-6900</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Гарганеева</surname><given-names>А. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Garganeeva</surname><given-names>A. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Гарганеева Алла Анатольевна - д-р мед. наук, профессор, заведующий отделением патологии миокарда, НИИ кардиологии Томского НИМЦ.</p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Alla A. Garganeeva - Dr. Sci. (Med.), Professor, Head of the Department of Myocardial Pathology, Cardiology Research Institute, Tomsk NRMC.</p><p>634012, Tomsk, Kievskaya str., 111a</p></bio><email xlink:type="simple">aag@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/0000-0001-6066-3998</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Афанасьев</surname><given-names>С. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Afanasiev</surname><given-names>S. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Афанасьев Сергей Александрович - д-р мед. наук, профессор, заведующий лабораторией молекулярно-клеточной патологии и генодиагностики, НИИ кардиологии Томского НИМЦ.</p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Sergey A. Afanasiev - Dr. Sci. (Med.), Professor, Head of the Laboratory of Molecular and Cellular Pathology and Gene Diagnostics, Cardiology Research Institute, Tomsk NRMC.</p><p>634012, Tomsk, Kievskaya str., 111a</p></bio><email xlink:type="simple">tursky@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, Russian Academy of Sciences (Cardiology Research Institute, Tomsk NRMC)</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2025</year></pub-date><pub-date pub-type="epub"><day>12</day><month>12</month><year>2025</year></pub-date><volume>40</volume><issue>4</issue><fpage>123</fpage><lpage>130</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Муслимова Э.Ф., Кужелева Е.А., Гарганеева А.А., Афанасьев С.А., 2025</copyright-statement><copyright-year>2025</copyright-year><copyright-holder xml:lang="ru">Муслимова Э.Ф., Кужелева Е.А., Гарганеева А.А., Афанасьев С.А.</copyright-holder><copyright-holder xml:lang="en">Muslimova E.F., Kuzheleva E.A., Garganeeva A.A., Afanasiev S.A.</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/2917">https://www.sibjcem.ru/jour/article/view/2917</self-uri><abstract><sec><title>Введение</title><p>Введение. Распространенные полиморфизмы митохондриальной ДНК (мтДНК) могут влиять на интенсивность клеточного дыхания и продукцию активных форм кислорода. Избыточное количество активных форм кислорода приводит к окислительному стрессу, который способствует развитию многофакторных заболеваний. Можно ожидать, что полиморфизмы мтДНК могут выступить как кандидатные локусы риска развития или прогрессирования сердечно-сосудистой патологии.</p></sec><sec><title>Цель исследования</title><p>Цель исследования: оценка ассоциации полиморфизмов мтДНК C7028T, G3010A и G9055A с тяжестью течения хронической сердечной недостаточности (ХСН) у пациентов с ишемической болезнью сердца (ИБС).</p></sec><sec><title>Материал и методы</title><p>Материал и методы. В выборку включены 97 пациентов в возрасте 63 (58; 68) лет. Перенесенный в анамнезе инфаркт миокарда (ИМ) диагностирован у 74 (76,3%) пациентов. Выполнены стандартные клинико-инструментальные методы исследования. Определены полиморфизмы мтДНК с помощью полимеразной цепной реакции (ПЦР) с последующим анализом полиморфизма длин рестрикционных фрагментов.</p></sec><sec><title>Результаты</title><p>Результаты. Выявлено, что среди пациентов с умеренно сниженной фракцией выброса (ФВ) аллель 7028T встречался в 2 раза чаще, чем среди пациентов с сохраненной и низкой ФВ (78,9 против 34,3% и 34,9%, p = 0,002). При низкой ФВ среди пациентов с дилатацией правого предсердия (ПП) частота аллеля 7028С составила 8 (44,4%), аллеля 7028T – 10 (55,6%); без дилатации – 20 (80,0%) и 5 (20,0%) (p = 0,024). Отсутствовала ассоциация между полиморфизмом G3010A и параметрами, характеризующими тяжесть течения ХСН. Но частота аллеля 3010A была меньше среди пациентов с потребностью в диуретической терапии, чем среди лиц, не принимавших диуретики (8,6 против 30,8%, p = 0,005). Только у 3 (3,1%) больных установлен аллель 9055A.</p></sec><sec><title>Заключение</title><p>Заключение. Среди пациентов с ХСН ишемического генеза выявлена ассоциация полиморфизма C7028T мтДНК с фенотипом ХСН с умеренно сниженной ФВ левого желудочка (ЛЖ), при низкой ФВ – с дилатацией ПП. Полиморфизм G3010A мтДНК продемонстрировал ассоциацию с частотой применения диуретических препаратов.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Introduction</title><p>Introduction. Common mitochondrial DNA (mtDNA) polymorphisms can affect the intensity of cellular respiration and the production of reactive oxygen species. Excessive amounts of reactive oxygen species lead to oxidative stress, which contributes to the development of multifactorial diseases. It can be expected that mtDNA polymorphisms can act as candidate risk loci for the development or progression of cardiovascular pathology.</p></sec><sec><title>Aim</title><p>Aim: To evaluate the association of mtDNA polymorphisms C7028T, G3010A and G9055A with the severity of chronic heart failure (CHF) in patients with ischemic heart disease.</p></sec><sec><title>Material and Methods</title><p>Material and Methods. The sample included 97 patients aged 63 (58; 68) years. A history of myocardial infarction was diagnosed in 74 (76.3%) patients. Standard clinical and instrumental research methods were performed. The mtDNA polymorphisms were determined using polymerase chain reaction followed by restriction fragment length polymorphism analysis.</p></sec><sec><title>Results</title><p>Results. It was found that among patients with a moderately reduced ejection fraction, the 7028T allele was found 2 times more often than among patients with preserved and reduced ejection fraction (EF) (78.9% versus 34.3% and 34.9%, p = 0.002). In patients with low EF and right atrial dilation, the frequency of the 7028C allele was 8 (44.4%), the 7028T allele – 10 (55.6%); without dilation – 20 (80.0%) and 5 (20.0%) (p = 0.024). There was no association between the G3010A polymorphism and parameters characterizing the severity of CHF. However, the frequency of 3010A substitution was lower among patients requiring diuretic therapy than among those not taking diuretics (8.6% vs. 30.8%, p = 0.005). Only 3 patients (3.1%) were identified with the 9055A allele.</p></sec><sec><title>Conclusion</title><p>Conclusion. Among patients with CHF of ischemic genesis, an association of mtDNA C7028T polymorphism with a heart failure phenotype with a moderately reduced left ventricular EF and in group with low EF with right atrial dilation was revealed. The mtDNA G3010A polymorphism was associated with a diuretic prescription.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>митохондриальная ДНК</kwd><kwd>полиморфизм</kwd><kwd>хроническая сердечная недостаточность</kwd><kwd>фракция выброса</kwd><kwd>ишемическая болезнь сердца</kwd></kwd-group><kwd-group xml:lang="en"><kwd>mitochondrial DNA</kwd><kwd>polymorphism</kwd><kwd>chronic heart failure</kwd><kwd>ejection fraction</kwd><kwd>ischemic heart disease</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">исследование выполнено за счет гранта Российского научного фонда (проект № 23-7500009)</funding-statement><funding-statement xml:lang="en">the study was supported by a grant from the Russian Science Foundation (project № 23-7500009)</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">Wallace D.C. Mitochondria as chi. Genetics. 2008;179(2):727–735. https://doi.org/10.1534/genetics.104.91769</mixed-citation><mixed-citation xml:lang="en">Wallace D.C. Mitochondria as chi. Genetics. 2008;179(2):727–735. https://doi.org/10.1534/genetics.104.91769</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Poznyak A.V., Ivanova E.A., Sobenin I.A., Yet S.-F., Orekhov A.N. The role of mitochondria in cardiovascular diseases. Biology. 2020;9(6):137. https://doi.org/10.3390/biology9060137</mixed-citation><mixed-citation xml:lang="en">Poznyak A.V., Ivanova E.A., Sobenin I.A., Yet S.-F., Orekhov A.N. The role of mitochondria in cardiovascular diseases. Biology. 2020;9(6):137. https://doi.org/10.3390/biology9060137</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Gori T., Münzel T. Oxidative stress and endothelial dysfunction: Therapeutic implications. Ann. Med. 2011;43(4):259–272. https://doi.org/10.3109/07853890.2010.543920</mixed-citation><mixed-citation xml:lang="en">Gori T., Münzel T. Oxidative stress and endothelial dysfunction: Therapeutic implications. Ann. Med. 2011;43(4):259–272. https://doi.org/10.3109/07853890.2010.543920</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Mohammed S.A., Ambrosini S., Lüscher T., Paneni F., Costantino S. Epigenetic сontrol of mitochondrial function in the vasculature. Front. Cardiovasc. Med. 2020;7:28. https://doi.org/10.3389/fcvm.2020.00028</mixed-citation><mixed-citation xml:lang="en">Mohammed S.A., Ambrosini S., Lüscher T., Paneni F., Costantino S. Epigenetic сontrol of mitochondrial function in the vasculature. Front. Cardiovasc. Med. 2020;7:28. https://doi.org/10.3389/fcvm.2020.00028</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Li Y., Liu X. Novel insights into the role of mitochondrial fusion and fission in cardiomyocyte apoptosis induced by ischemia/reperfusion. J. Cellular Physiology. 2018;233(8):5589–5597. https://doi.org/10.1002/jcp.26522</mixed-citation><mixed-citation xml:lang="en">Li Y., Liu X. Novel insights into the role of mitochondrial fusion and fission in cardiomyocyte apoptosis induced by ischemia/reperfusion. J. Cellular Physiology. 2018;233(8):5589–5597. https://doi.org/10.1002/jcp.26522</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Martínez-Redondo D., Marcuello A., Casajús J.A., Ara I., Dahmani Y., Montoya J. et al. Human mitochondrial haplogroup H: The highest VO2max consumer – is it a paradox? Mitochondrion. 2010;10(2):102–107. https://doi.org/10.1016/j.mito.2009.11.005</mixed-citation><mixed-citation xml:lang="en">Martínez-Redondo D., Marcuello A., Casajús J.A., Ara I., Dahmani Y., Montoya J. et al. Human mitochondrial haplogroup H: The highest VO2max consumer – is it a paradox? Mitochondrion. 2010;10(2):102–107. https://doi.org/10.1016/j.mito.2009.11.005</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Голубенко М.В., Шумакова Т.В., Макеева О.А., Тарасенко Н.В., Салахов Р.Р., Шипулин В.М. и др. Полиморфизм митохондриальной ДНК и ишемия миокарда: ассоциация гаплогруппы Н с сердечной недостаточностью. Сибирский журнал клинической и экспериментальной медицины. 2021;36(4):70–77. https://doi.org/10.29001/20738552-2021-36-4-70-77</mixed-citation><mixed-citation xml:lang="en">Golubenko M.V., Shumakova T.V., Makeeva O.A., Tarasenko N.V., Salakhov R.R., Shipulin V.M. et al. Mitochondrial DNA polymorphism and myocardial ischemia: Association of haplogroup H with heart failure. Siberian Journal of Clinical and Experimental Medicine. 2021;36(4):70–77. (In Russ.). https://doi.org/10.29001/2073-8552-2021-36-4-70-77</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Luppi E., De Luise M., Bini C., Pelletti G., Tioli G., Kurelac I. et al. The landscape of rare mitochondrial DNA variants in sudden cardiac death: A potential role for ATP synthase. Heliyon. 2025;11(1):e41592. https://doi.org/10.1016/j.heliyon.2024.e41592</mixed-citation><mixed-citation xml:lang="en">Luppi E., De Luise M., Bini C., Pelletti G., Tioli G., Kurelac I. et al. The landscape of rare mitochondrial DNA variants in sudden cardiac death: A potential role for ATP synthase. Heliyon. 2025;11(1):e41592. https://doi.org/10.1016/j.heliyon.2024.e41592</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Ganetzky R.D., Stendel C., McCormick E.M., Zolkipli-Cunningham Z., Goldstein A.C., Klopstock T. et al. MT-ATP6 mitochondrial disease variants: Phenotypic and biochemical features analysis in 218 published cases and cohort of 14 new cases. Human Mutation. 2019;40:499–515. https://doi.org/10.1002/humu.23723</mixed-citation><mixed-citation xml:lang="en">Ganetzky R.D., Stendel C., McCormick E.M., Zolkipli-Cunningham Z., Goldstein A.C., Klopstock T. et al. MT-ATP6 mitochondrial disease variants: Phenotypic and biochemical features analysis in 218 published cases and cohort of 14 new cases. Human Mutation. 2019;40:499–515. https://doi.org/10.1002/humu.23723</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Heidari M.M., Khatami M., Kamalipour A., Kalantari M., Movahed M., Emmamy M.H. et al. Mitochondrial mutations in protein coding genes of respiratory chain including complexes IV, V, and mt-tRNA genes are associated risk factors for congenital heart disease. EXCLI J. 2022;21:1306–1330. https://doi.org/10.17179/excli2022-5298</mixed-citation><mixed-citation xml:lang="en">Heidari M.M., Khatami M., Kamalipour A., Kalantari M., Movahed M., Emmamy M.H. et al. Mitochondrial mutations in protein coding genes of respiratory chain including complexes IV, V, and mt-tRNA genes are associated risk factors for congenital heart disease. EXCLI J. 2022;21:1306–1330. https://doi.org/10.17179/excli2022-5298</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Scheffer D.L., Garcia A.A., Lee L., Mochly-Rosen D., Ferreira J.C.B. Mitochondrial fusion, fission, and mitophagy in cardiac diseases: Challenges and therapeutic opportunities. Antioxid Redox Signal. 2022;36(13-15):844–863. https://doi.org/10.1089/ars.2021.0145</mixed-citation><mixed-citation xml:lang="en">Scheffer D.L., Garcia A.A., Lee L., Mochly-Rosen D., Ferreira J.C.B. Mitochondrial fusion, fission, and mitophagy in cardiac diseases: Challenges and therapeutic opportunities. Antioxid Redox Signal. 2022;36(13-15):844–863. https://doi.org/10.1089/ars.2021.0145</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Domínguez-Garrido E., Martínez-Redondo D., Martín-Ruiz C., Gómez-Durán A., Ruiz-Pesini E., Madero P. et al. Association of mitochondrial haplogroup J and mtDNA oxidative damage in two different North Spain elderly populations. Biogerontology. 2009;10:435–442. https://doi.org/10.1007/s10522-008-9186-y</mixed-citation><mixed-citation xml:lang="en">Domínguez-Garrido E., Martínez-Redondo D., Martín-Ruiz C., GómezDurán A., Ruiz-Pesini E., Madero P. et al. Association of mitochondrial haplogroup J and mtDNA oxidative damage in two different North Spain elderly populations. Biogerontology. 2009;10:435–442. https://doi.org/10.1007/s10522-008-9186-y</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Wallace D.C. Bioenergetics in human evolution and disease: implications for the origins of biological complexity and the missing genetic variation of common diseases. Philos. Trans. R. Soc. Lond. B. Biol. Sci. 2013;368(1622):20120267. https://doi.org/10.1098/rstb.2012.0267</mixed-citation><mixed-citation xml:lang="en">Wallace D.C. Bioenergetics in human evolution and disease: implications for the origins of biological complexity and the missing genetic variation of common diseases. Philos. Trans. R. Soc. Lond. B. Biol. Sci. 2013;368(1622):20120267. https://doi.org/10.1098/rstb.2012.0267</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Atabekov T., Korepanov V., Krivolapov S., Khlynin M., Afanasiev S., Golubenko M. et al. Mitochondrial DNA polymorphisms of peripheral blood mononuclear cells associated with sustained ventricular tachycardia in patients with cardioverter-defibrillator implantation indications. Rev. Cardiovasc. Med. 2025;26(3):26744. https://doi.org/10.31083/RCM26744</mixed-citation><mixed-citation xml:lang="en">Atabekov T., Korepanov V., Krivolapov S., Khlynin M., Afanasiev S., Golubenko M. et al. Mitochondrial DNA polymorphisms of peripheral blood mononuclear cells associated with sustained ventricular tachycardia in patients with cardioverter-defibrillator implantation indications. Rev. Cardiovasc. Med. 2025;26(3):26744. https://doi.org/10.31083/RCM26744</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Minasyan L., Sreekumar P.G., Hinton D.R., Kannan R. Protective mechanisms of the mitochondrial-derived peptide humanin in oxidative and endoplasmic reticulum stress in RPE cells. Oxid. Med. Cell Longev. 2017;2017:1675230. https://doi.org/10.1155/2017/1675230</mixed-citation><mixed-citation xml:lang="en">Minasyan L., Sreekumar P.G., Hinton D.R., Kannan R. Protective mechanisms of the mitochondrial-derived peptide humanin in oxidative and endoplasmic reticulum stress in RPE cells. Oxid. Med. Cell Longev. 2017;2017:1675230. https://doi.org/10.1155/2017/1675230</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Cobb L.J., Lee C., Xiao J., Yen K., Wong R.G., Nakamura H.K. et al. Naturally occurring mitochondrial-derived peptides are age-dependent regulators of apoptosis, insulin sensitivity, and inflammatory markers. Aging (Albany NY). 2016;8(4):796–809. https://doi.org/10.18632/aging.100943</mixed-citation><mixed-citation xml:lang="en">Cobb L.J., Lee C., Xiao J., Yen K., Wong R.G., Nakamura H.K. et al. Naturally occurring mitochondrial-derived peptides are age-dependent regulators of apoptosis, insulin sensitivity, and inflammatory markers. Aging (Albany NY). 2016;8(4):796–809. https://doi.org/10.18632/aging.100943</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Bai R-K., Leal S.M., Covarrubias D., Liu A., Wong L.-J.C. Mitochondrial genetic background modifies breast cancer risk. Cancer Res. 2007;67(10):4687–4694. https://doi.org/10.1158/0008-5472.CAN-06-3554</mixed-citation><mixed-citation xml:lang="en">Bai R-K., Leal S.M., Covarrubias D., Liu A., Wong L.-J.C. Mitochondrial genetic background modifies breast cancer risk. Cancer Res. 2007;67(10):4687–4694. https://doi.org/10.1158/0008-5472.CAN-06-3554</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Castañeda V., Haro-Vinueza A., Salinas I., Caicedo A., Méndez M.Á. The MitoAging Project: Single nucleotide polymorphisms (SNPs) in mitochondrial genes and their association to longevity. Mitochondrion. 2022;66:13–26. https://doi.org/10.1016/j.mito.2022.06.008</mixed-citation><mixed-citation xml:lang="en">Castañeda V., Haro-Vinueza A., Salinas I., Caicedo A., Méndez M.Á. The MitoAging Project: Single nucleotide polymorphisms (SNPs) in mitochondrial genes and their association to longevity. Mitochondrion. 2022;66:13–26. https://doi.org/10.1016/j.mito.2022.06.008</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Шляхтина Н.В., Антоненок Е.А., Галанцев А.О. Клинико-патогенетические особенности хронической сердечной недостаточности с промежуточной фракцией выброса. Сибирский журнал клинической и экспериментальной медицины. 2021;36(3):45–50. https://doi.org/10.29001/2073-8552-2021-36-3-45-50</mixed-citation><mixed-citation xml:lang="en">Shlyakhtina N.V., Antonenok E.A., Galantsev A.O. Clinical and pathogenetic features of chronic heart failure with mid-range ejection fraction. Siberian Journal of Clinical and Experimental Medicine. 2021;36(3):45–50. (In Russ.). https://doi.org/10.29001/2073-8552-2021-36-3-45-50</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Kirichenko T.V., Sobenin I.A., Khasanova Z.B., Orekhova V.A., Melnichenko A.A., Demakova N.A. et al. Data on association of mitochondrial heteroplasmy and cardiovascular risk factors: Comparison of samples from Russian and Mexican populations. Data in Brief. 2018;18:16–21. https://doi.org/10.1016/j.dib.2018.02.068</mixed-citation><mixed-citation xml:lang="en">Kirichenko T.V., Sobenin I.A., Khasanova Z.B., Orekhova V.A., Melnichenko A.A., Demakova N.A. et al. Data on association of mitochondrial heteroplasmy and cardiovascular risk factors: Comparison of samples from Russian and Mexican populations. Data in Brief. 2018;18:16–21. https://doi.org/10.1016/j.dib.2018.02.068</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>
