pmjТихоокеанский медицинский журналPacific Medical Journal1609-1175TGMU10.34215/1609-1175-2022-1-10-16pmj-2295Research ArticleОБЗОРЫREVIEWSДисфункция митохондрий и сосудистое старение при коморбидной патологииMitochondrial dysfunction and vascular aging in comorbid pathologyhttps://orcid.org/0000-0002-0117-0349НевзороваВ. А.NevzorovaV. A.

Невзорова Вера Афанасьевна - доктор медицинских наук, профессор, директор института терапии и инструментальной диагностики.

690002, Владивосток, пр-т Острякова, 2

Vera A. Nevzorova - MD (Medicine), PhD, Professor, Director of Institute of Therapy and Instrumental Diagnostics.

2 Ostryakova Ave. Vladivostok 690002

nevzorova@inbox.ruhttps://orcid.org/0000-0002-1107-4561ЧертокВ. М.ChertokV. M.

Черток Виктор Михайлович – доктор медицинских наук, профессор, заведующий кафедрой анатомии человека.

690002, Владивосток, пр-т Острякова, 2

Victor M. Chertok - MD, PhD, professor, Head of Human Anatomy Department.

2 Ostryakova Ave., Vladivostok, 690002

chertokv@mail.ruhttps://orcid.org/0000-0002-9836-6339БродскаяТ. А.BrodskayaT. A.

Бродская Татьяна Александровна - доктор медицинских наук, профессор, директор Департамента клинической медицины Школы медицины ФГАОУ ДФУ; профессор института терапии и инструментальной диагностики Тихоокеанского ГМУ.

690922 Владивосток, о. Русский, п. Аякс, 10$ 690002, Владивосток, пр-т Острякова, 2

Tatiana A. Brodskaya - MD (Medicine), PhD, Professor, Director of Department of Clinical Medicine, School of Medicine, Far Eastern FU; Professor of Institute of Therapy and Instrumental Diagnostics, Pacific SMU.

10 Ajax Bay, Russky Island, Vladivostok, 690922; 2 Ostryakova Ave. Vladivostok 690002

brodskaya.ta@dvfu.ruhttps://orcid.org/0000-0002-3632-9575СелюковаП. А.SelyukovaP. A.

Селюкова Полина Александровна - аспирант института терапии и инструментальной диагностики.

690002, Владивосток, пр-т Острякова, 2

Polina A. Selyukova - graduate student, Institute of Therapy and Instrumental Diagnostics.

2 Ostryakova Ave. Vladivostok 690002

polina.selyukova@gmail.comhttps://orcid.org/0000-0002-5809-3989ЗахарчукН. В.ZakharchukN. V.

Захарчук Наталья Владимировна (автор по переписки) - доктор медицинских наук, профессор института терапии и инструментальной диагностики.

690002, Владивосток, пр-т Острякова, 2

Natalia V. Zakharchuk - MD (Medicine), PhD, Professor of Institute of Therapy and Instrumental Diagnostics.

2 Ostryakova Ave. Vladivostok 690002

zaharchuknat@mail.ruТихоокеанский государственный медицинский университетРоссияPacific State Medical UniversityRussian FederationТихоокеанский государственный медицинский университет; Дальневосточный федеральный университетРоссияPacific State Medical University; Far Eastern Federal UniversityRussian Federation202225032022011016Copyright © Невзорова В.А., Черток В.М., Бродская Т.А., Селюкова П.А., Захарчук Н.В., 20222022Невзорова В.А., Черток В.М., Бродская Т.А., Селюкова П.А., Захарчук Н.В.Nevzorova V.A., Chertok V.M., Brodskaya T.A., Selyukova P.A., Zakharchuk N.V.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.tmj-vgmu.ru/jour/article/view/2295

Сердечно-сосудистые заболевания занимают лидирующие позиции в структуре смертности современного общества. Для большинства данных заболеваний характерны неконтролируемые процессы оксидативного стресса, протеолиза, тканевой и клеточной гипоксии, вызывающие эндотелиальную дисфункцию. Тканевая и клеточная гипоксия с накоплением митохондриальных реактивных форм кислорода, повреждающих липопротеиды, белки, нуклеиновые кислоты, является краеугольным камнем теории свободнорадикального окисления в патогенезе сосудистого старения. Особенностью «состаренного» фенотипа клеток является уменьшение числа митохондрий, снижение количества копий митохондриальной ДНК и потеря митохондриального белка в тканях. Помимо морфологических изменений, угнетается функция митохондрий, ослабевает активность их белков и ферментов. Изменения функций митохондрий могут быть вторичными в ответ на различные стимулы и связаны с нарушением их структуры и ослаблением активности в ответ на особые генетические и фенотипические условия. Перепрограммирование митохондриального биогенеза занимает центральную позицию в различных теориях развития ускоренного старения и служит одной из привлекательных мишеней для возможных вмешательств в продлении активного долголетия.

Cardiovascular diseases take a leading position in the structure of mortality in modern society. Most diseases are characterized by uncontrolled processes of oxidative stress, proteolysis, tissue and cellular hypoxia, which cause endothelial dysfunction. Tissue and cellular hypoxia accumulated with mitochondrial reactive forms of oxygen damaging lipoproteins, proteins, nucleic acids plays an important role in the pathogenesis of vascular aging. Cellular aging is characterized by a decrease in the number of mitochondria, a decrease in the number of copies of mitochondrial DNA, and the loss of mitochondrial protein. In addition to morphological changes, the function of mitochondria is oppressed, at the same time the activity of their proteins and enzymes decreases. Changes in the functions of mitochondria can be secondary in response to various stimuli and are associated with a violation of their structure and a change in activity in response to specific genetic and phenotypic conditions. Reprogramming of mitochondrial biogenesis occupies a central position in the theory of cellular aging and is one of the targets for interventions in prolonging active longevity.

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The authors declare that there are no conflicts of interest present.