Патоморфогенез гипертрофической кардиомиопатии заключается в нарушении расположения пучков мышечных клеток в миокарде и ассоциирован с мутациями генов, кодирующих синтез сократительных белков миокарда. Метаболические изменения при этой патологии обусловлены гипертрофией межжелудочковой перегородки вследствие нарушения работы сократительного аппарата миокарда, связанного с данными мутациями, а также дисфункцией митохондрий. Мутации белков миофибрилл могут негативно влиять на митохондрии посредством повышенного окислительного стресса из-за увеличенной потребности в АТФ. Митохондрии являются сложно устроенными органеллами с собственной кольцевой ДНК, а также характеризуются наличием ферментных комплексов, участвующих в окислительно-восстановительных реакциях, что обусловливает частое повреждение митохондриальных белковых структур и мембран активными формами кислорода. В связи с этим дисфункция митохондрий также может быть вызвана мутациями в генах, кодирующих митохондриальные белки, что приводит к нарушению митофагии и митохондриальной динамики. Функционирование дефектных митохондрий связано с недостаточным синтезом аденозинтрифосфата и неэффективным мышечным сокращением, что приводит на уровне ткани к тем же последствиям, что и мутации генов сократительных белков.

В настоящем обзоре мы постарались обобщить роль митохондриальной дисфункции в патоморфогенезе гипертрофической кардиомиопатии.

hypertrophic cardiomyopathymitochondriamitochondrial dysfunctionгипертрофическая кардиомиопатиямитохондриимитохондриальная дисфункцияРоссийский Научный ФондRussian Science Foundation23-75-100261.Litt MJ, Ali A, Reza N. Familial hypertrophic cardiomyopathy: diagnosis and management. Vasc Health Risk Manag. 2023;19:211–221. doi: 10.2147/VHRM.S365001Litt M.J., Ali A., Reza N. Familial hypertrophic cardiomyopathy: diagnosis and management // Vasc Health Risk Manag. 2023. Vol. 19. P. 211–221. doi: 10.2147/VHRM.S3650012.Kozlova MA, Areshidze DA, Chernikov VP, et al. Ultrastructural characteristics of myocardial mitochondria in hypertrophic cardiomyopathy with diffuse-generalized phenotype. Clinical and Experimental Surgery. Petrovsky Journal. 2024;12(1):7–14. EDN: YSAODE doi: 10.33029/2308-1198-2024-12-1-7-14Козлова М.А., Арешидзе Д. А., Черников В. П., и др. Ультраструктурные характеристики митохондрий миокарда при гипертрофической кардиомиопатии диффузно-генерализованного фенотипа // Клиническая и экспериментальная хирургия. Журнал имени академика Б. В. Петровского. 2024. Т. 12, № 1. С. 7–14. EDN: YSAODE doi: 10.33029/2308-1198-2024-12-1-7-143.Rhee TM, Kim HK, Kim BS, et al. Impact of coronary artery revascularization on long-term outcome in hypertrophic cardiomyopathy patients: a nationwide population-based cohort study. Sci Rep. 2023;13(1):6412. doi: 10.1038/s41598-023-33344-3Rhee T.M., Kim H. K., Kim B. S., et al. Impact of coronary artery revascularization on long-term outcome in hypertrophic cardiomyopathy patients: a nationwide population-based cohort study // Sci Rep. 2023. Vol. 13, N 1. P. 6412. doi: 10.1038/s41598-023-33344-34.Gabrusenko SA, Gudkova AYa, Koziolova NA, et al. 2020 clinical practice guidelines for hypertrophic cardiomyopathy. Russian Journal of Cardiology. 2021;26(5):269–334. EDN: MXDYLE doi: 10.15829/1560-4071-2021-4541Габрусенко С.А., Гудкова А. Я., Козиолова Н. А., и др. Гипертрофическая кардиомиопатия. Клинические рекомендации 2020 // Российский кардиологический журнал. 2021. T. 26, № 5. С. 269–334. EDN: MXDYLE doi: 10.15829/1560-4071-2021-45415.Mojumder J, Fan L, Nguyen T, et al. Computational analysis of ventricular mechanics in hypertrophic cardiomyopathy patients. Sci Rep. 2023;13(1):958. doi: 10.1038/s41598-023-28037-wMojumder J., Fan L., Nguyen T., et al. Computational analysis of ventricular mechanics in hypertrophic cardiomyopathy patients // Sci Rep. 2023. Vol. 13, N 1. P. 958. doi: 10.1038/s41598-023-28037-w6.Reza N, De Feria A, Wang T, et al. Left ventricular hypertrophy and hypertrophic cardiomyopathy in adult solid organ transplant recipients. Transplant Direct. 2021;8(1):e1279. doi: 10.1097/TXD.0000000000001279Reza N., De Feria A., Wang T., et al. Left ventricular hypertrophy and hypertrophic cardiomyopathy in adult solid organ transplant recipients // Transplant Direct. 2021. Vol. 8, N 1. P. e1279. doi: 10.1097/TXD.00000000000012797.Sexton M, Westaby J, Zullo E, Sheppard MN. Fatal case of hypertrophic cardiomyopathy in a donor heart: a case report. Transplant Proc. 2022;54(10):2703–2704. doi: 10.1016/j.transproceed.2022.10.038Sexton M., Westaby J., Zullo E., et al. Fatal case of hypertrophic cardiomyopathy in a donor heart: a case report // Transplant Proc. 2022. Vol. 54, N 10. P. 2703–2704. doi: 10.1016/j.transproceed.2022.10.0388.Pollmann K, Kaltenecker E, Schleihauf J, et al. Compound mutation in cardiac sarcomere proteins is associated with increased risk for major arrhythmic events in pediatric onset hypertrophic cardiomyopathy. J Clin Med. 2021;10(22):5256. doi: 10.3390/jcm10225256.Pollmann K., Kaltenecker E., Schleihauf J., et al. Compound mutation in cardiac sarcomere proteins is associated with increased risk for major arrhythmic events in pediatric onset hypertrophic cardiomyopathy // J Clin Med. 2021. Vol. 10, N 22. P. 5256. doi: 10.3390/jcm102252569.Bick AG, Wakimoto H, Kamer KJ, et al. Cardiovascular homeostasis dependence on MICU2, a regulatory subunit of the mitochondrial calcium uniporter. Proc Natl Acad Sci U S A. 2017;114(43):E9096–E9104. doi: 10.1073/pnas.1711303114Bick A.G., Wakimoto H., Kamer K. J., et al. Cardiovascular homeostasis dependence on MICU2, a regulatory subunit of the mitochondrial calcium uniporter // Proc Natl Acad Sci U S A. 2017. Vol. 114, N 43. P. E9096–E9104. doi: 10.1073/pnas.171130311410.Chowdhury SAK, Warren CM, Simon JN, et al. Modifications of sarcoplasmic reticulum function prevent progression of sarcomere-linked hypertrophic cardiomyopathy despite a persistent increase in myofilament calcium response. Front Physiol. 2020;11:107. doi: 10.3389/fphys.2020.00107Chowdhury S.A.K., Warren C. M., Simon J. N., et al. Modifications of sarcoplasmic reticulum function prevent progression of sarcomere-linked hypertrophic cardiomyopathy despite a persistent increase in myofilament calcium response // Front Physiol. 2020. Vol. 11. P. 107. doi: 10.3389/fphys.2020.0010711.Lombardi M, Lazzeroni D, Pisano A, et al. Mitochondrial energetics and Ca2+-activated ATPase in obstructive hypertrophic cardiomyopathy. J Clin Med. 2020;9(6):1799. doi: 10.3390/jcm9061799Lombardi M., Lazzeroni D., Pisano A., et al. Mitochondrial energetics and Ca2+-activated atpase in obstructive hypertrophic cardiomyopathy // J Clin Med. 2020. Vol. 9, N 6. P. 1799. doi: 10.3390/jcm906179912.Cohn R, Thakar K, Lowe A, et al. A contraction stress model of hypertrophic cardiomyopathy due to sarcomere mutations. Stem Cell Reports. 2019;12(1):71–83. doi: 10.1016/j.stemcr.2018.11.015Cohn R., Thakar K., Lowe A., et al. A contraction stress model of hypertrophic cardiomyopathy due to sarcomere mutations // Stem Cell Reports. 2019. Vol. 12, N 1. P. 71–83. doi: 10.1016/j.stemcr.2018.11.01513.Lorenzini M, Norrish G, Field E, et al. Penetrance of hypertrophic cardiomyopathy in sarcomere protein mutation carriers. J Am Coll Cardiol. 2020;76(5):550–559. doi: 10.1016/j.jacc.2020.06.011Lorenzini M., Norrish G., Field E., et al. Penetrance of hypertrophic cardiomyopathy in sarcomere protein mutation carriers // J Am Coll Cardiol. 2020. Vol. 76, N 5. P. 550–559. doi: 10.1016/j.jacc.2020.06.01114.Chou C, Chin MT. Pathogenic mechanisms of hypertrophic cardiomyopathy beyond sarcomere dysfunction. Int J Mol Sci. 2021;22(16):8933. doi: 10.3390/ijms22168933Chou C., Chin M. T. Pathogenic mechanisms of hypertrophic cardiomyopathy beyond sarcomere dysfunction // Int J Mol Sci. 2021. Vol. 22, N 16. P. 8933. doi: 10.3390/ijms2216893315.Joy G, Kelly CI, Webber M, et al. Microstructural and microvascular phenotype of sarcomere mutation carriers and overt hypertrophic cardiomyopathy. Circulation. 2023;148(10):808–818. doi: 10.1161/CIRCULATIONAHA.123.063835Joy G., Kelly C. I., Webber M., et al. Microstructural and microvascular phenotype of sarcomere mutation carriers and overt hypertrophic cardiomyopathy // Circulation. 2023. Vol. 148, N 10. P. 808–818. doi: 10.1161/CIRCULATIONAHA.123.06383516.Tudurachi BS, Zăvoi A, Leonte A, et al. An update on MYBPC3 gene mutation in hypertrophic cardiomyopathy. Int J Mol Sci. 2023;24(13):10510. doi: 10.3390/ijms241310510Tudurachi B.S., Zăvoi A., Leonte A., et al. An update on MYBPC3 gene mutation in hypertrophic cardiomyopathy // Int J Mol Sci. 2023. Vol. 24, N 13. P. 10510. doi: 10.3390/ijms24131051017.García-Vielma C, Lazalde-Córdova LG, Arzola-Hernández JC, et al. Identification of variants in genes associated with hypertrophic cardiomyopathy in Mexican patients. Mol Genet Genomics. 2023;298(6):1289–1299. doi: 10.1007/s00438-023-02048-8 Erratum in: Mol Genet Genomics. 2023;298(6):1593. doi: 10.1007/s00438-023-02069-3García-Vielma C., Lazalde-Córdova L.G., Arzola-Hernández J.C., et al. Identification of variants in genes associated with hypertrophic cardiomyopathy in Mexican patients // Mol Genet Genomics. 2023. Vol. 298, N 6. P. 1593. doi: 10.1007/s00438-023-02048-8 Erratum in: Mol Genet Genomics. 2023. Vol. 298, N 6. P. 1289–1299. doi: 10.1007/s00438-023-02069-318.Güvenç O, Karaer K, Haydin S, et al. Implantation of cardiac defibrillator in an infant with hypertrophic cardiomyopathy and newly identified MYBP3 mutation. Turk Pediatri Ars. 2020;55(3):304–308. doi: 10.14744/TurkPediatriArs.2018.35556Güvenç O., Karaer K., Haydin S., et al. Implantation of cardiac defibrillator in an infant with hypertrophic cardiomyopathy and newly identified MYBP3 mutation // Turk Pediatri Ars. 2020. Vol. 55, N 3. P. 304–308. doi: 10.14744/TurkPediatriArs.2018.3555619.Dong Y, Li X, Fu W, et al. Generation of an iPSC line (ZZUNEUi021-A) from a hypertrophic cardiomyopathy patient with TNNT2 mutation. Stem Cell Res. 2022;58:102622. doi: 10.1016/j.scr.2021.102622Dong Y., Li X., Fu W., et al. Generation of an iPSC line (ZZUNEUi021-A) from a hypertrophic cardiomyopathy patient with TNNT2 mutation // Stem Cell Res. 2022. Vol. 58. P. 102622. doi: 10.1016/j.scr.2021.10262220.Kim H, Kim HJ, Oh J, et al. An induced pluripotent stem cell line (YCMi006-A) generated from a patient with hypertrophic cardiomyopathy who carries the ACTA1 mutation p.Ile343Met. Stem Cell Res. 2022;63:102874. doi: 10.1016/j.scr.2022.102874Kim H., Kim H. J., Oh J., et al. An induced pluripotent stem cell line (YCMi006-A) generated from a patient with hypertrophic cardiomyopathy who carries the ACTA1 mutation p.Ile343Met // Stem Cell Res. 2022. Vol. 63. P. 102874. doi: 10.1016/j.scr.2022.10287421.Zhao SR, Shen M, Lee C, et al. Generation of three induced pluripotent stem cell lines from hypertrophic cardiomyopathy patients carrying TNNI3 mutations. Stem Cell Res. 2021;57:102597. doi: 10.1016/j.scr.2021.102597Zhao S.R., Shen M., Lee C., et al. Generation of three induced pluripotent stem cell lines from hypertrophic cardiomyopathy patients carrying TNNI3 mutations // Stem Cell Res. 2021. Vol. 57. P. 102597. doi: 10.1016/j.scr.2021.10259722.Wijnker PJ, Friedrich FW, Dutsch A, et al. Comparison of the effects of a truncating and a missense MYBPC3 mutation on contractile parameters of engineered heart tissue. J Mol Cell Cardiol. 2016;97:82–92. doi: 10.1016/j.yjmcc.2016.03.003Wijnker P.J.M., Friedrich F. W., Dutsch A., et al. Comparison of the effects of a truncating and a missense MYBPC3 mutation on contractile parameters of engineered heart tissue // J Mol Cell Cardiol. 2016. Vol. 97. P. 82–92. doi: 10.1016/j.yjmcc.2016.03.00323.Meijering RA, Henning RH, Brundel BJ. Reviving the protein quality control system: therapeutic target for cardiac disease in the elderly. Trends Cardiovasc Med. 2015;25(3):243–247. doi: 10.1016/j.tcm.2014.10.013Meijering R.A.M., Henning R. H., Brundel B. J. Reviving the protein quality control system: therapeutic target for cardiac disease in the elderly // Trends Cardiovasc Med. 2015. Vol. 25, N 3. P. 243–247. doi: 10.1016/j.tcm.2014.10.01324.Sequeira V, Wijnker PJ, Nijenkamp LL, et al. Perturbed length-dependent activation in human hypertrophic cardiomyopathy with missense sarcomeric gene mutations. Circ Res. 2013;112(11):1491–505. Corrected and republished from: Circ Res. 2013;113(8):e87. doi: 10.1161/CIRCRESAHA.111.300436Sequeira V., Wijnker P. J.M., Nijenkamp L. L., et al. Perturbed length-dependent activation in human hypertrophic cardiomyopathy with missense sarcomeric gene mutations // Circ Res. 2013. Vol. 112, N 11. P. 1491–1505. Corrected and republished from: Circ Res. 2013. Vol. 113, N 8. P. e87. doi: 10.1161/CIRCRESAHA.111.30043625.Wijnker PJM, Sequeira V, Kuster DWD, Velden JV. Hypertrophic cardiomyopathy: a vicious cycle triggered by sarcomere mutations and secondary disease hits. Antioxid Redox Signal. 2019;31(4):318–358. doi: 10.1089/ars.2017.7236Wijnker P.J.M., Sequeira V., Kuster D. W.D., Velden J. V. Hypertrophic cardiomyopathy: a vicious cycle triggered by sarcomere mutations and secondary disease hits // Antioxid Redox Signal. 2019. Vol. 31, N 4. P. 318–358. doi: 10.1089/ars.2017.723626.Witjas-Paalberends ER, Ferrara C, Scellini B, et al. Faster cross-bridge detachment and increased tension cost in human hypertrophic cardiomyopathy with the R403Q MYH7 mutation. J Physiol. 2014;592(15):3257–3272. doi: 10.1113/jphysiol.2014.274571Witjas-Paalberends E.R., Ferrara C., Scellini B., et al. Faster cross-bridge detachment and increased tension cost in human hypertrophic cardiomyopathy with the R403Q MYH7 mutation // J Physiol. 2014. Vol. 592, N 15. P. 3257–3272. doi: 10.1113/jphysiol.2014.27457127.Belus A, Piroddi N, Scellini B, et al. The familial hypertrophic cardiomyopathy-associated myosin mutation R403Q accelerates tension generation and relaxation of human cardiac myofibrils. J Physiol. 2008;586(15):3639–3644. doi: 10.1113/jphysiol.2008.155952Belus A., Piroddi N., Scellini B., et al. The familial hypertrophic cardiomyopathy-associated myosin mutation R403Q accelerates tension generation and relaxation of human cardiac myofibrils // J Physiol. 2008. Vol. 586, N 15. P. 3639–3644. doi: 10.1113/jphysiol.2008.15595228.Anmann T, Eimre M, Kuznetsov AV, et al. Calcium-induced contraction of sarcomeres changes the regulation of mitochondrial respiration in permeabilized cardiac cells. FEBS J. 2005;272(12):3145–3161. doi: 10.1111/j.1742-4658.2005.04734.xAnmann T., Eimre M., Kuznetsov A. V., et al. Calcium-induced contraction of sarcomeres changes the regulation of mitochondrial respiration in permeabilized cardiac cells // FEBS J. 2005. Vol. 272, N 12. P. 3145–3161. doi: 10.1111/j.1742-4658.2005.04734.x29.Singh SR, Kadioglu H, Patel K, et al. Is Desmin propensity to aggregate part of its protective function? Cells. 2020;9(2):491. doi: 10.3390/cells9020491Singh S.R., Kadioglu H., Patel K., et al. Is Desmin propensity to aggregate part of its protective function? // Cells. 2020. Vol. 9, N 2. P. 491. doi: 10.3390/cells902049130.Taylor MR, Slavov D, Ku L, et al. Prevalence of desmin mutations in dilated cardiomyopathy. Circulation. 2007;115(10):1244–1251. doi: 10.1161/CIRCULATIONAHA.106.646778Taylor M.R.G., Slavov D., Ku L., et al. Prevalence of desmin mutations in dilated cardiomyopathy // Circulation. 2007. Vol. 115, N 10. P. 1244–1251. doi: 10.1161/CIRCULATIONAHA.106.64677831.Li Y, Zhang W, Dai Y, Chen K. Identification and verification of IGFBP3 and YTHDC1 as biomarkers associated with immune infiltration and mitophagy in hypertrophic cardiomyopathy. Front Genet. 2022;13:986995. doi: 10.3389/fgene.2022.986995Li Y., Zhang W., Dai Y., Chen K. Identification and verification of IGFBP3 and YTHDC1 as biomarkers associated with immune infiltration and mitophagy in hypertrophic cardiomyopathy // Front Genet. 2022. Vol. 13. P. 986995. doi: 10.3389/fgene.2022.98699532.Vakrou S, Abraham MR. Hypertrophic cardiomyopathy: a heart in need of an energy bar? Front Physiol. 2014;5:309. doi: 10.3389/fphys.2014.00309Vakrou S., Abraham M. R. Hypertrophic cardiomyopathy: a heart in need of an energy bar? // Front Physiol. 2014. Vol. 5. P. 309. doi: 10.3389/fphys.2014.0030933.Brambilla A, Olivotto I, Favilli S, et al. Impact of cardiovascular involvement on the clinical course of paediatric mitochondrial disorders. Orphanet J Rare Dis. 2020;15(1):196. doi: 10.1186/s13023–020–01466-wBrambilla A., Olivotto I., Favilli S., et al. Impact of cardiovascular involvement on the clinical course of paediatric mitochondrial disorders // Orphanet J Rare Dis. 2020. Vol. 15, N 1. P. 196. doi: 10.1186/s13023–020–01466-w34.Gehmlich K, Dodd MS, Allwood JW, et al. Changes in the cardiac metabolome caused by perhexiline treatment in a mouse model of hypertrophic cardiomyopathy. Mol Biosyst. 2015;11(2):564–573. doi: 10.1039/c4mb00594eGehmlich K., Dodd M. S., William Allwood J., et al. Changes in the cardiac metabolome caused by perhexiline treatment in a mouse model of hypertrophic cardiomyopathy // Mol Biosyst. 2015. Vol. 11, N 2. P. 564–573. doi: 10.1039/c4mb00594e35.Chung H, Kim Y, Cho SM, et al. Differential contributions of sarcomere and mitochondria-related multigene variants to the endophenotype of hypertrophic cardiomyopathy. Mitochondrion. 2020;53:48–56. doi: 10.1016/j.mito.2020.04.010Chung H., Kim Y., Cho S. M., et al. Differential contributions of sarcomere and mitochondria-related multigene variants to the endophenotype of hypertrophic cardiomyopathy // Mitochondrion. 2020. Vol. 53. P. 48–56. doi: 10.1016/j.mito.2020.04.01036.Giacomello M, Pyakurel A, Glytsou C, Scorrano L. The cell biology of mitochondrial membrane dynamics. Nat Rev Mol Cell Biol. 2020;21(4):204–224. doi: 10.1038/s41580-020-0210-7Giacomello M., Pyakurel A., Glytsou C., Scorrano L. The cell biology of mitochondrial membrane dynamics // Nature Reviews Molecular Cell Biology. 2020. Vol. 21, N 4. P. 204–224. doi: 10.1038/s41580-020-0210-737.Frye RE, Lionnard L, Singh I, et al. Mitochondrial morphology is associated with respiratory chain uncoupling in autism spectrum disorder. Transl Psychiatry. 2021;11(1):527. doi: 10.1038/s41398-021-01647-6Frye R.E., Lionnard L., Singh I., et al. Mitochondrial morphology is associated with respiratory chain uncoupling in autism spectrum disorder // Transl Psychiatry. 2021. Vol. 11, N 1. P. 527. doi: 10.1038/s41398-021-01647-638.Chiang S, Braidy N, Maleki S, et al. Mechanisms of impaired mitochondrial homeostasis and NAD+ metabolism in a model of mitochondrial heart disease exhibiting redox active iron accumulation. Redox Biol. 2021;46:102038. doi: 10.1016/j.redox.2021.102038Chiang S., Braidy N., Maleki S., et al. Mechanisms of impaired mitochondrial homeostasis and NAD+ metabolism in a model of mitochondrial heart disease exhibiting redox active iron accumulation // Redox Biol. 2021. Vol. 46. P. 102038. doi: 10.1016/j.redox.2021.10203839.Tokuyama T, Yanagi S. Role of mitochondrial dynamics in heart diseases. Genes (Basel). 2023;14(10):1876. doi: 10.3390/genes14101876Tokuyama T., Yanagi S. Role of mitochondrial dynamics in heart diseases // Genes (Basel). 2023. Vol. 14, N 10. P. 1876. doi: 10.3390/genes1410187640.Hovhannisyan Y, Li Z, Callon D, et al. Critical contribution of mitochondria in the development of cardiomyopathy linked to desmin mutation. Stem Cell Res Ther. 2024;15(1):10. doi: 10.1186/s13287-023-03619-7Hovhannisyan Y., Li Z., Callon D., et al. Critical contribution of mitochondria in the development of cardiomyopathy linked to desmin mutation // Stem Cell Res Ther. 2024. Vol. 15, N 1. P. 10. doi: 10.1186/s13287-023-03619-741.Vučković S, Dinani R, Nollet EE, et al. Characterization of cardiac metabolism in iPSC-derived cardiomyocytes: lessons from maturation and disease modeling. Stem Cell Res Ther. 2022;13(1):332. doi: 10.1186/s13287-022-03021-9Vučković S., Dinani R., Nollet E. E., et al. Characterization of cardiac metabolism in iPSC-derived cardiomyocytes: lessons from maturation and disease modeling // Stem Cell Res Ther. 2022. Vol. 13, N 1. P. 332. doi: 10.1186/s13287-022-03021-942.Abdullah CS, Remex NS, Aishwarya R, et al. Mitochondrial dysfunction and autophagy activation are associated with cardiomyopathy developed by extended methamphetamine self-administration in rats. Redox Biol. 2022;58:102523. doi: 10.1016/j.redox.2022.102523Abdullah C.S., Remex N. S., Aishwarya R., et al. Mitochondrial dysfunction and autophagy activation are associated with cardiomyopathy developed by extended methamphetamine self-administration in rats // Redox Biol. 2022. Vol. 58. P. 102523. doi: 10.1016/j.redox.2022.10252343.Peoples JN, Saraf A, Ghazal N, et al. Mitochondrial dysfunction and oxidative stress in heart disease. Exp Mol Med. 2019;51(12):1–13. doi: 10.1038/s12276-019-0355-7Peoples J.N., Saraf A., Ghazal N., et al. Mitochondrial dysfunction and oxidative stress in heart disease // Exp Mol Med. 2019. Vol. 51, N 12. P. 1–13. doi: 10.1038/s12276-019-0355-744.Zhi F, Zhang Q, Liu L, et al. Novel insights into the role of mitochondria in diabetic cardiomyopathy: molecular mechanisms and potential treatments. Cell Stress Chaperones. 2023;28(6):641–655. doi: 10.1007/s12192-023-01361-wZhi F., Zhang Q., Liu L., et al. Novel insights into the role of mitochondria in diabetic cardiomyopathy: molecular mechanisms and potential treatments // Cell Stress Chaperones. 2023. Vol. 28, N 6. P. 641–655. doi: 10.1007/s12192-023-01361-w45.Friederich MW, Geddes GC, Wortmann SB, et al. Pathogenic variants in MRPL44 cause infantile cardiomyopathy due to a mitochondrial translation defect. Mol Genet Metab. 2021;133(4):362–371. doi: 10.1016/j.ymgme.2021.06.001Friederich M.W., Geddes G. C., Wortmann S. B., et al. Pathogenic variants in MRPL44 cause infantile cardiomyopathy due to a mitochondrial translation defect // Mol Genet Metab. 2021. Vol. 133, N 4. P. 362–371. doi: 10.1016/j.ymgme.2021.06.00146.Li S, Pan H, Tan C, et al. Mitochondrial dysfunctions contribute to hypertrophic cardiomyopathy in patient iPSC-derived cardiomyocytes with MT-RNR2 mutation. Stem Cell Reports. 2018;10(3):808–821. doi: 10.1016/j.stemcr.2018.01.013Li S., Pan H., Tan C., et al. Mitochondrial dysfunctions contribute to hypertrophic cardiomyopathy in patient iPSC-derived cardiomyocytes with MT-RNR2 mutation // Stem Cell Reports. 2018. Vol. 10, N 3. P. 808–821. doi: 10.1016/j.stemcr.2018.01.01347.Sharma S, Bhattarai S, Ara H, et al. SOD2 deficiency in cardiomyocytes defines defective mitochondrial bioenergetics as a cause of lethal dilated cardiomyopathy. Redox Biol. 2020;37:101740. doi: 10.1016/j.redox.2020.101740Sharma S., Bhattarai S., Ara H., et al. SOD2 deficiency in cardiomyocytes defines defective mitochondrial bioenergetics as a cause of lethal dilated cardiomyopathy // Redox Biol. 2020. Vol. 37. P. 101740. doi: 10.1016/j.redox.2020.10174048.Alam S, Abdullah CS, Aishwarya R, et al. Dysfunctional mitochondrial dynamic and oxidative phosphorylation precedes cardiac dysfunction in R120G-αB-crystallin-induced desmin-related cardiomyopathy. J Am Heart Assoc. 2020;9(23):e017195. doi: 10.1161/JAHA.120.017195Alam S., Abdullah C. S., Aishwarya R., et al. Dysfunctional mitochondrial dynamic and oxidative phosphorylation precedes cardiac dysfunction in R120G-αB-crystallin-induced desmin-related cardiomyopathy // J Am Heart Assoc. 2020. Vol. 9, N 23. P. e017195. doi: 10.1161/JAHA.120.01719549.Ranjbarvaziri S, Kooiker KB, Ellenberger M, et al. Altered cardiac energetics and mitochondrial dysfunction in hypertrophic cardiomyopathy. Circulation. 2021;144(21):1714–1731. doi: 10.1161/CIRCULATIONAHA.121.053575Ranjbarvaziri S., Kooiker K. B., Ellenberger M., et al. Altered cardiac energetics and mitochondrial dysfunction in hypertrophic cardiomyopathy // Circulation. 2021. Vol. 144, N 21. P. 1714–1731. doi: 10.1161/CIRCULATIONAHA.121.05357550.Shimada BK, Boyman L, Huang W, et al. Pyruvate-driven oxidative phosphorylation is downregulated in sepsis-induced cardiomyopathy: a study of mitochondrial proteome. Shock. 2022;57(4):553–564. doi: 10.1097/SHK.0000000000001858Shimada B.K., Boyman L., Huang W., et al. Pyruvate-driven oxidative phosphorylation is downregulated in sepsis-induced cardiomyopathy: a study of mitochondrial proteome // Shock. 2022. Vol. 57, N 4. P. 553–564. doi: 10.1097/SHK.000000000000185851.Maltês S, Lopes LR. New perspectives in the pharmacological treatment of hypertrophic cardiomyopathy. Novas perspetivas no tratamento farmacológico da miocardiopatia hipertrófica. Rev Port Cardiol (Engl Ed). 2020;39(2):99–109. doi: 10.1016/j.repc.2019.03.008Maltês S., Lopes L. R. Novas perspetivas no tratamento farmacológico da miocardiopatia hipertrófica // Rev Port Cardiol (Engl Ed). 2020. Vol. 39, N 2. P. 99–109. doi: 10.1016/j.repc.2019.03.00852.Kuan SW, Chua KH, Tan EW, et al. Whole mitochondrial genome sequencing of Malaysian patients with cardiomyopathy. PeerJ. 2022;10:e13265. doi: 10.7717/peerj.13265Kuan S.W., Chua K. H., Tan E. W., et al. Whole mitochondrial genome sequencing of Malaysian patients with cardiomyopathy // PeerJ. 2022. Vol. 10. P. e13265. doi: 10.7717/peerj.1326553.Ding Y, Gao B, Huang J. Mitochondrial cardiomyopathy: the roles of mt-tRNA mutations. J Clin Med. 2022;11(21):6431. doi: 10.3390/jcm11216431Ding Y., Gao B., Huang J. Mitochondrial cardiomyopathy: the roles of mt-tRNA mutations // J Clin Med. 2022. Vol. 11, N 21. P. 6431. doi: 10.3390/jcm1121643154.Solomon T, Filipovska A, Hool L, Viola H. Preventative therapeutic approaches for hypertrophic cardiomyopathy. J Physiol. 2021;599(14):3495–3512. doi: 10.1113/JP279410Solomon T., Filipovska A., Hool L., Viola H. Preventative therapeutic approaches for hypertrophic cardiomyopathy // J Physiol. 2021. Vol. 599, N 14. P. 3495–3512. doi: 10.1113/JP27941055.Wu B, Li J, Ni H, et al. TLR4 activation promotes the progression of experimental autoimmune myocarditis to dilated cardiomyopathy by inducing mitochondrial dynamic imbalance. Oxid Med Cell Longev. 2018;2018:3181278. doi: 10.1155/2018/3181278Wu B., Li J., Ni H., et al. TLR4 Activation promotes the progression of experimental autoimmune myocarditis to dilated cardiomyopathy by inducing mitochondrial dynamic imbalance // Oxid Med Cell Longev. 2018. Vol. 2018. P. 3181278. doi: 10.1155/2018/318127856.Kang C, Badr MA, Kyrychenko V, et al. Deficit in PINK1/PARKIN-mediated mitochondrial autophagy at late stages of dystrophic cardiomyopathy. Cardiovasc Res. 2018;114(1):90–102. doi: 10.1093/cvr/cvx201Kang C., Badr M. A., Kyrychenko V., et al. Deficit in PINK1/PARKIN-mediated mitochondrial autophagy at late stages of dystrophic cardiomyopathy // Cardiovasc Res. 2018. Vol. 114, N 1. P. 90–102. doi: 10.1093/cvr/cvx20157.Andres AM, Tucker KC, Thomas A, et al. Mitophagy and mitochondrial biogenesis in atrial tissue of patients undergoing heart surgery with cardiopulmonary bypass. JCI Insight. 2017;2(4):e89303. doi: 10.1172/jci.insight.89303Andres A.M., Tucker K. C., Thomas A., et al. Mitophagy and mitochondrial biogenesis in atrial tissue of patients undergoing heart surgery with cardiopulmonary bypass // JCI Insight. 2017. Vol. 2, N 4. P. e89303. doi: 10.1172/jci.insight.8930358.Hsiao YT, Shimizu I, Wakasugi T, et al. Cardiac mitofusin-1 is reduced in non-responding patients with idiopathic dilated cardiomyopathy. Sci Rep. 2021;11(1):6722. doi: 10.1038/s41598-021-86209-yHsiao Y.T., Shimizu I., Wakasugi T., et al. Cardiac mitofusin-1 is reduced in non-responding patients with idiopathic dilated cardiomyopathy // Sci Rep. 2021. Vol. 11, N 1. P. 6722. doi: 10.1038/s41598-021-86209-y59.Chen H, Ren S, Clish C, et al. Titration of mitochondrial fusion rescues Mff-deficient cardiomyopathy. J Cell Biol. 2015;211(4):795–805. doi: 10.1083/jcb.201507035Chen H., Ren S., Clish C., et al. Titration of mitochondrial fusion rescues Mff-deficient cardiomyopathy // J Cell Biol. 2015. Vol. 211, N 4. P. 795–805. doi: 10.1083/jcb.20150703560.Spiegel R, Saada A, Flannery PJ, et al. Fatal infantile mitochondrial encephalomyopathy, hypertrophic cardiomyopathy and optic atrophy associated with a homozygous OPA1 mutation. J Med Genet. 2016;53(2):127–131. doi: 10.1136/jmedgenet-2015-103361Spiegel R., Saada A., Flannery P. J., et al. Fatal infantile mitochondrial encephalomyopathy, hypertrophic cardiomyopathy and optic atrophy associated with a homozygous OPA1 mutation // J Med Genet. 2016. Vol. 53, N 2. P. 127–131. doi: 10.1136/jmedgenet-2015-10336161.Zhuang Q, Guo F, Fu L, et al. 1-Deoxynojirimycin promotes cardiac function and rescues mitochondrial cristae in mitochondrial hypertrophic cardiomyopathy. J Clin Invest. 2023;133(14):e164660. doi: 10.1172/JCI164660Zhuang Q., Guo F., Fu L., et al. 1-Deoxynojirimycin promotes cardiac function and rescues mitochondrial cristae in mitochondrial hypertrophic cardiomyopathy // J Clin Invest. 2023. Vol. 133, N 14. P. e164660. doi: 10.1172/JCI16466062.AlTamimi JZ, AlFaris NA, Alshammari GM, et al. The protective effect of 11-Keto-β-boswellic acid against diabetic cardiomyopathy in rats entails activation of AMPK. Nutrients. 2023;15(7):1660. doi: 10.3390/nu15071660AlTamimi J.Z., AlFaris N.A., Alshammari G. M., et al. The protective effect of 11-Keto-β-boswellic acid against diabetic cardiomyopathy in rats entails activation of AMPK // Nutrients. 2023. Vol. 15, N 7. P. 1660. doi: 10.3390/nu1507166063.Albasher G, Alkahtani S, Al-Harbi LN. Urolithin A prevents streptozotocin-induced diabetic cardiomyopathy in rats by activating SIRT1. Saudi J Biol Sci. 2022;29(2):1210–1220. doi: 10.1016/j.sjbs.2021.09.045Albasher G., Alkahtani S., Al-Harbi L. N. Urolithin A prevents streptozotocin-induced diabetic cardiomyopathy in rats by activating SIRT1 // Saudi J Biol Sci. 2022. Vol. 29, N 2. P. 1210–1220. doi: 10.1016/j.sjbs.2021.09.04564.Viola HM, Hool LC. Impaired calcium handling and mitochondrial metabolic dysfunction as early markers of hypertrophic cardiomyopathy. Arch Biochem Biophys. 2019;665:166–174. doi: 10.1016/j.abb.2019.03.006Viola H.M., Hool L. C. Impaired calcium handling and mitochondrial metabolic dysfunction as early markers of hypertrophic cardiomyopathy // Arch Biochem Biophys. 2019. Vol. 665, P. 166–174. doi: 10.1016/j.abb.2019.03.00665.Klawitter F, Ehler J, Bajorat R, Patejdl R. Mitochondrial dysfunction in intensive care unit-acquired weakness and critical illness myopathy: a narrative review. Int J Mol Sci. 2023;24(6):5516. doi: 10.3390/ijms24065516Klawitter F., Ehler J., Bajorat R., et al. Mitochondrial dysfunction in intensive care unit-acquired weakness and critical illness myopathy: a narrative review // Int J Mol Sci. 2023. Vol. 24, N 6. P. 5516. doi: 10.3390/ijms2406551666.Moore J, Ewoldt J, Venturini G, et al. Multi-omics profiling of hypertrophic cardiomyopathy reveals altered mechanisms in mitochondrial dynamics and excitation-contraction coupling. Int J Mol Sci. 2023;24(5):4724. doi: 10.3390/ijms24054724Moore J., Ewoldt J., Venturini G., et al. Multi-omics profiling of hypertrophic cardiomyopathy reveals altered mechanisms in mitochondrial dynamics and excitation-contraction coupling // Int J Mol Sci. 2023. Vol. 24, N 5. P. 4724. doi: 10.3390/ijms2405472467.Tolstik TV, Kirichenko TV, Bogatyreva AI, et al. The role of mitochondrial dysfunction in the pathogenesis of inflammatory diseases. Journal of Atherosclerosis and Dyslipidemias. 2023;(3):10–17. EDN: PBLRHI doi: 10.34687/2219–8202.JAD.2023.03.0002Толстик Т.В., Кириченко Т. В., Богатырева А. И., и др. Роль дисфункции митохондрий в патогенезе воспалительных заболеваний и атеросклероза // Атеросклероз и дислипидемии. 2023. № 52. Р. 10–17. EDN: PBLRHI doi: 10.34687/2219-8202.JAD.2023.03.000268.Ma KY, Fokkens MR, Reggiori F, et al. Parkinson’s disease-associated VPS35 mutant reduces mitochondrial membrane potential and impairs PINK1/Parkin-mediated mitophagy. Transl Neurodegener. 2021;10(1):19. doi: 10.1186/s40035-021-00243-4Ma K.Y., Fokkens M. R., Reggiori F., et al. Parkinson’s disease-associated VPS35 mutant reduces mitochondrial membrane potential and impairs PINK1/Parkin-mediated mitophagy // Transl Neurodegener. 2021. Vol. 10, N 1. P. 19. doi: 10.1186/s40035-021-00243-469.Xu Y, Li Y. Regulatory effect of PINK1/Parkin axis on mitophagy in isoniazide-induced hepatocellular injury. Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2022;47(9):1200–1207. doi: 10.11817/j.issn.1672-7347.2022.210407Xu Y., Li Y. Regulatory effect of PINK1/Parkin axis on mitophagy in isoniazide-induced hepatocellular injury // Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2022. Vol. 47, N 9. P. 1200–1207. doi: 10.11817/j.issn.1672–7347.2022.21040770.Lu Y, Li Z, Zhang S, et al. Cellular mitophagy: mechanism, roles in diseases and small molecule pharmacological regulation. Theranostics. 2023;13(2):736–766. doi: 10.7150/thno.79876Lu Y., Li Z., Zhang S., et al. Cellular mitophagy: mechanism, roles in diseases and small molecule pharmacological regulation // Theranostics. 2023. Vol. 13, N 2. P. 736–766. doi: 10.7150/thno.7987671.Liu X, Ye B, Miller S, et al. Ablation of ALCAT1 mitigates hypertrophic cardiomyopathy through effects on oxidative stress and mitophagy. Mol Cell Biol. 2012;32(21):4493–4504. doi: 10.1128/MCB.01092–12Liu X., Ye B., Miller S., et al. Ablation of ALCAT1 mitigates hypertrophic cardiomyopathy through effects on oxidative stress and mitophagy // Mol Cell Biol. 2012. Vol. 32, N 21. P. 4493–4504. doi: 10.1128/MCB.01092–1272.Ahola S, Langer T. Ferroptosis in mitochondrial cardiomyopathy. Trends Cell Biol. 2024;34(2):150–160. doi: 10.1016/j.tcb.2023.06.002Ahola S., Langer T. Ferroptosis in mitochondrial cardiomyopathy // Trends Cell Biol. 2024. Vol. 34, N 2. P. 150–160. doi: 10.1016/j.tcb.2023.06.00273.Lin LF, Jhao YT, Chiu CH, et al. Bezafibrate exerts neuroprotective effects in a rat model of sporadic Alzheimer’s disease. Pharmaceuticals (Basel). 2022;15(2):109. doi: 10.3390/ph15020109Lin L.F., Jhao Y.T., Chiu C. H. et al. Bezafibrate exerts neuroprotective effects in a rat model of sporadic Alzheimer’s disease // Pharmaceuticals (Basel). 2022. Vol. 15, N 2. P. 109. doi: 10.3390/ph1502010974.Lyu J, Zhao Y, Zhang N, et al. Bezafibrate rescues mitochondrial encephalopathy in mice via induction of daily torpor and hypometabolic state. Neurotherapeutics. 2022;19(3):994–1006. doi: 10.1007/s13311-022-01216-9Lyu J., Zhao Y., Zhang N., et al. Bezafibrate rescues mitochondrial encephalopathy in mice via induction of daily torpor and hypometabolic state // Neurotherapeutics. 2022. Vol. 19, N 3. P. 994–1006. doi: 10.1007/s13311-022-01216-975.Grings M, Moura AP, Parmeggiani B, et al. Bezafibrate prevents mitochondrial dysfunction, antioxidant system disturbance, glial reactivity and neuronal damage induced by sulfite administration in striatum of rats: implications for a possible therapeutic strategy for sulfite oxidase deficiency. Biochim Biophys Acta Mol Basis Dis. 2017;1863(9):2135–2148. doi: 10.1016/j.bbadis.2017.05.019Grings M., Moura A. P., Parmeggiani B., et al. Bezafibrate prevents mitochondrial dysfunction, antioxidant system disturbance, glial reactivity and neuronal damage induced by sulfite administration in striatum of rats: Implications for a possible therapeutic strategy for sulfite oxidase deficiency // Biochim Biophys Acta Mol Basis Dis. 2017. Vol. 1863, N 9. P. 2135–2148. doi: 10.1016/j.bbadis.2017.05.01976.Zingerman B, Ziv D, Feder Krengel N, et al. Cessation of Bezafibrate in patients with chronic kidney disease improves renal function. Sci Rep. 2020;10(1):19768. doi: 10.1038/s41598-020-76861-1Zingerman B., Ziv D., Feder Krengel N., et al. Cessation of Bezafibrate in patients with chronic kidney disease improves renal function // Sci Rep. 2020. Vol. 10, N 1. P. 19768. doi: 10.1038/s41598-020-76861-177.Suyama T, Shimura M, Fushimi T, et al. Efficacy of Bezafibrate in two patients with mitochondrial trifunctional protein deficiency. Mol Genet Metab Rep. 2020;24:100610. doi: 10.1016/j.ymgmr.2020.100610Suyama T., Shimura M., Fushimi T., et al. Efficacy of bezafibrate in two patients with mitochondrial trifunctional protein deficiency // Mol Genet Metab Rep. 2020. Vol. 24. P. 100610. doi: 10.1016/j.ymgmr.2020.10061078.Kawakami R, Matsui H, Matsui M, et al. Empagliflozin induces the transcriptional program for nutrient homeostasis in skeletal muscle in normal mice. Sci Rep. 2023;13(1):18025. doi: 10.1038/s41598-023-45390-yKawakami R., Matsui H., Matsui M., et al. Empagliflozin induces the transcriptional program for nutrient homeostasis in skeletal muscle in normal mice // Sci Rep. 2023. Vol. 13, N 1. P. 18025. doi: 10.1038/s41598-023-45390-y79.Haileselassie B, Mukherjee R, Joshi AU, et al. Drp1/Fis1 interaction mediates mitochondrial dysfunction in septic cardiomyopathy. J Mol Cell Cardiol. 2019;130:160–169. doi: 10.1016/j.yjmcc.2019.04.006 Erratum in: J Mol Cell Cardiol. 2024;187:120. doi: 10.1016/j.yjmcc.2023.11.004Haileselassie B., Mukherjee R., Joshi A. U., et al. Drp1/Fis1 interaction mediates mitochondrial dysfunction in septic cardiomyopathy // J Mol Cell Cardiol. 2019. Vol. 130. P. 160–169. doi: 10.1016/j.yjmcc.2019.04.006 Erratum in: J Mol Cell Cardiol. 2024. Vol. 187. P. 120. doi: 10.1016/j.yjmcc.2023.11.00480.Nhu NT, Li Q, Liu Y, et al. Effects of Mdivi-1 on neural mitochondrial dysfunction and mitochondria-mediated apoptosis in ischemia-reperfusion injury after stroke: a systematic review of preclinical studies. Front Mol Neurosci. 2021;14:778569. doi: 10.3389/fnmol.2021.778569Nhu N.T., Li Q., Liu Y., et al. Effects of Mdivi-1 on neural mitochondrial dysfunction and mitochondria-mediated apoptosis in ischemia-reperfusion injury after stroke: a systematic review of preclinical studies // Front Mol Neurosci. 2021. Vol. 14. P. 778569. doi: 10.3389/fnmol.2021.77856981.Chen Y, Li S, Guo Y, et al. Astaxanthin attenuates hypertensive vascular remodeling by protecting vascular smooth muscle cells from oxidative stress-induced mitochondrial dysfunction. Oxid Med Cell Longev. 2020. Vol. 2020. P. 4629189. doi: 10.1155/2020/4629189 Erratum in: Oxid Med Cell Longev. 2021;2021:9796134. doi: 10.1155/2021/9796134Chen Y., Li S., Guo Y., et al. Astaxanthin attenuates hypertensive vascular remodeling by protecting vascular smooth muscle cells from oxidative stress-induced mitochondrial dysfunction // Oxid Med Cell Longev. 2020. Vol. 2020. P. 4629189. doi: 10.1155/2020/4629189 Erratum in: Oxid Med Cell Longev. 2021. Vol. 2021. P. 9796134. doi: 10.1155/2021/979613482.Osgerby L, Lai YC, Thornton PJ, et al. Kinetin riboside and its ProTides activate the Parkinson’s disease associated PTEN-induced putative kinase 1 (PINK1) independent of mitochondrial depolarization. J Med Chem. 2017;60(8):3518–3524. doi: 10.1021/acs.jmedchem.6b01897Osgerby L., Lai Y. C., Thornton P. J., et al. Kinetin riboside and Its ProTides activate the Parkinson’s disease associated PTEN-induced putative kinase 1 (PINK1) independent of mitochondrial depolarization // J Med Chem. 2017. Vol. 60, N 8. P. 3518–3524. doi: 10.1021/acs.jmedchem.6b0189783.Borah JC, Mujtaba S, Karakikes I, et al. A small molecule binding to the coactivator CREB-binding protein blocks apoptosis in cardiomyocytes. Chem Biol. 2011;18(4):531–541. doi: 10.1016/j.chembiol.2010.12.021Borah J.C., Mujtaba S., Karakikes I., et al. A small molecule binding to the coactivator CREB-binding protein blocks apoptosis in cardiomyocytes // Chem Biol. 2011. Vol. 18, N 4. P. 531–541. doi: 10.1016/j.chembiol.2010.12.02184.Adisa RA, Sulaimon LA, Okeke EG, et al. Mitoquinol mesylate (MITOQ) attenuates diethyl nitrosamine-induced hepatocellular carcinoma through modulation of mitochondrial antioxidant defense systems. Toxicol Res. 2021;38(3):275–291. doi: 10.1007/s43188-021-00105-1Adisa R.A., Sulaimon L. A., Okeke E. G., et al. Mitoquinol mesylate (MITOQ) attenuates diethyl nitrosamine-induced hepatocellular carcinoma through modulation of mitochondrial antioxidant defense systems // Toxicol Res. 2021. Vol. 38, N 3. P. 275–291. doi: 10.1007/s43188-021-00105-185.Russo S, De Rasmo D, Signorile A, et al. Beneficial effects of SS-31 peptide on cardiac mitochondrial dysfunction in tafazzin knockdown mice. Sci Rep. 2022;12(1):19847. doi: 10.1038/s41598-022-24231-4Russo S., De Rasmo D., Signorile A., et al. Beneficial effects of SS-31 peptide on cardiac mitochondrial dysfunction in tafazzin knockdown mice // Sci Rep. 2022. Vol. 12, N 1. P. 19847. doi: 10.1038/s41598-022-24231-486.Vockley J. Long-chain fatty acid oxidation disorders and current management strategies. Am J Manag Care. 2020;26(7 Suppl.): S147-S154. doi: 10.37765/ajmc.2020.88480Vockley J. Long-chain fatty acid oxidation disorders and current management strategies // Am J Manag Care. 2020. Vol. 26 (Suppl 7). P. S147–S154. doi: 10.37765/ajmc.2020.8848087.Wang J, Huang X, Liu H, et al. Empagliflozin ameliorates diabetic cardiomyopathy via attenuating oxidative stress and improving mitochondrial function. Oxid Med Cell Longev. 2022;2022:1122494. doi: 10.1155/2022/1122494Wang J., Huang X., Liu H., et al. Empagliflozin ameliorates diabetic cardiomyopathy via attenuating oxidative stress and improving mitochondrial function // Oxid Med Cell Longev. 2022. Vol. 2022. P. 1122494. doi: 10.1155/2022/112249488.Zhou J, Pang J, Tripathi M, et al. Spermidine-mediated hypusination of translation factor EIF5A improves mitochondrial fatty acid oxidation and prevents non-alcoholic steatohepatitis progression. Nat Commun. 2022;13(1):5202. doi: 10.1038/s41467-022-32788-xZhou J., Pang J., Tripathi M., et al. Spermidine-mediated hypusination of translation factor EIF5A improves mitochondrial fatty acid oxidation and prevents non-alcoholic steatohepatitis progression // Nat Commun. 2022. Vol. 13, N 1. P. 5202. doi: 10.1038/s41467-022-32788-x89.Messerer J, Wrede C, Schipke J, et al. Spermidine supplementation influences mitochondrial number and morphology in the heart of aged mice. J Anat. 2023;242(1):91–101. doi: 10.1111/joa.13618Messerer J., Wrede C., Schipke J., et al. Spermidine supplementation influences mitochondrial number and morphology in the heart of aged mice // J Anat. 2023. Vol. 242. P. 91–101. doi: 10.1111/joa.1361890.Chai N, Zheng H, Zhang H, et al. Spermidine alleviates intrauterine hypoxia-induced offspring newborn myocardial mitochondrial damage in rats by inhibiting oxidative stress and regulating mitochondrial quality control. Iran J Pharm Res. 2023;21(1):e133776. doi: 10.5812/ijpr-133776Chai N., Zheng H., Zhang H., et al. Spermidine alleviates intrauterine hypoxia-induced offspring newborn myocardial mitochondrial damage in rats by inhibiting oxidative stress and regulating mitochondrial quality control // Iran J Pharm Res. 2023. Vol. 21, N 1. P. e133776. doi: 10.5812/ijpr-13377691.Omar EM, Omar RS, Shoela MS, El Sayed NS. A study of the cardioprotective effect of spermidine: a novel inducer of autophagy. Chin J Physiol. 2021;64(6):281–288. doi: 10.4103/cjp.cjp_76_21Omar E., Omar R., Shoela M., et al. A study of the cardioprotective effect of spermidine: a novel inducer of autophagy // Chin J Physiol. 2021. Vol. 64. N 6. P. 281–288. doi: 10.4103/cjp.cjp_76_2192.Yan J, Yan JY, Wang YX, et al. Spermidine-enhanced autophagic flux improves cardiac dysfunction following myocardial infarction by targeting the AMPK/mTOR signalling pathway. Br J Pharmacol. 2019;176(17):3126–3142. doi: 10.1111/bph.14706Yan J., Yan J. Y., Wang Y. X., et al. Spermidine-enhanced autophagic flux improves cardiac dysfunction following myocardial infarction by targeting the AMPK/mTOR signalling pathway // Br J Pharmacol. 2019. Vol. 176, N 17. P. 3126–3142. doi: 10.1111/bph.1470693.Eisenberg T, Abdellatif M, Zimmermann A, et al. Dietary spermidine for lowering high blood pressure. Autophagy. 2017;13(4):767–769. doi: 10.1080/15548627.2017.1280225Eisenberg T., Abdellatif M., Zimmermann A., et al. Dietary spermidine for lowering high blood pressure // Autophagy. 2017. Vol. 13, N 4. P. 767–769. doi: 10.1080/15548627.2017.128022594.Liu S, Huang T, Liu R, et al. Spermidine suppresses development of experimental abdominal aortic aneurysms. J Am Heart Assoc. 2020;9(8):e014757. doi: 10.1161/JAHA.119.014757Liu S., Huang T., Liu R., et al. Spermidine suppresses development of experimental abdominal aortic aneurysms // J Am Heart Assoc. 2020. Vol. 9, N 8. P. e014757. doi: 10.1161/JAHA.119.01475795.Mosqueira D, Mannhardt I, Bhagwan JR, et al. CRISPR/Cas9 editing in human pluripotent stem cell-cardiomyocytes highlights arrhythmias, hypocontractility, and energy depletion as potential therapeutic targets for hypertrophic cardiomyopathy. Eur Heart J. 2018;39(43):3879–3892. doi: 10.1093/eurheartj/ehy249Mosqueira D., Mannhardt I., Bhagwan J. R., et al. CRISPR/Cas9 editing in human pluripotent stem cell-cardiomyocytes highlights arrhythmias, hypocontractility, and energy depletion as potential therapeutic targets for hypertrophic cardiomyopathy // Eur Heart J. 2018. Vol. 39, N 43. P. 3879–3892. doi: 10.1093/eurheartj/ehy24996.Liu L, Zhu J, Chen H, Hong L, Jiang J. Rediscovering the value of exercise in patients with hypertrophic cardiomyopathy. Zhejiang Da Xue Xue Bao Yi Xue Ban. 2022;51(6):758–764. doi: 10.3724/zdxbyxb-2022-0323Liu L., Zhu J., Chen H., et al. Rediscovering the value of exercise in patients with hypertrophic cardiomyopathy // Zhejiang Da Xue Xue Bao Yi Xue Ban. 2022. Vol. 51, N 6. P. 758–764. doi: 10.3724/zdxbyxb-2022-032397.Gusdon AM, Callio J, Distefano G, et al. Exercise increases mitochondrial complex I activity and DRP1 expression in the brains of aged mice. Exp Gerontol. 2017;90:1–13. doi: 10.1016/j.exger.2017.01.013Gusdon A.M., Callio J., Distefano G., et al. Exercise increases mitochondrial complex I activity and DRP1 expression in the brains of aged mice // Exp Gerontol. 2017. Vol. 90. P. 1–13. doi: 10.1016/j.exger.2017.01.01398.Pang R, Wang X, Pei F, et al. Regular exercise enhances cognitive function and intracephalic GLUT expression in Alzheimer’s disease model mice. J Alzheimers Dis. 2019;72(1):83–96. doi: 10.3233/JAD-190328Pang R., Wang X., Pei F., et al. Regular exercise enhances cognitive function and intracephalic GLUT expression in Alzheimer’s disease model mice // J Alzheimers Dis. 2019. Vol. 72, N 1. P. 83–96. doi: 10.3233/JAD-19032899.Pires RA, Correia TML, Almeida AA, et al. Time-course of redox status, redox-related, and mitochondrial-dynamics-related gene expression after an acute bout of different physical exercise protocols. Life (Basel). 2022;12(12):2113. doi: 10.3390/life12122113Pires R.A., Correia T. M.L., Almeida A. A., et al. Time-course of redox status, redox-related, and mitochondrial-dynamics-related gene expression after an acute bout of different physical exercise protocols // Life (Basel). 2022. Vol. 12, N 12. P. 2113. doi: 10.3390/life12122113