Роль митохондриальной дисфункции в развитии длительного COVID: обзорная статья

Авдеева К.С., Петелина Т.И., Горбачевский А.В., Бессонова М.И. Роль митохондриальной дисфункции в развитии длительного COVID: обзорная статья // CardioСоматика. 2025. Т. 16, № 4. С. 352–362. DOI: 10.17816/CS679567 EDN: FEFBCS

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Avdeeva KS, Petelina TI, Gorbachevskii AV, Bessonova MI. The Role of Mitochondrial Dysfunction in the Development of Long COVID: A Review. CardioSomatics. 2025;16(4):352–362. DOI: 10.17816/CS679567 EDN: FEFBCS

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Аннотация

Несмотря на завершение пандемии COVID-19, многие пациенты продолжают испытывать негативные последствия данного заболевания в виде кардиометаболических нарушений, а количество симптомов длительного COVID весьма многочисленно и разнообразно, что требует углубленного понимания механизмов данного заболевания. Одним из механизмов развития длительного COVID является транзиторная поствирусная митохондриальная дисфункция. Предполагается, что вирус SARS-CoV-2, прямо или опосредованно через системное воспаление, вызывает метаболическое перепрограммирование клеток, нарушая окислительное фосфорилирование, снижая продукцию АТФ и усиливая генерацию активных форм кислорода. При метаболическом перепрограммировании клетки предпочитают использовать гликолиз для выработки лактата. Высокий уровень лактата в крови при низкой интенсивности физической нагрузки указывает на митохондриальную дисфункцию. Кардиореспираторная выносливость напрямую связана с интегральной функцией многих систем и считается отражением общего состояния здоровья организма. Наиболее объективным и точным показателем кардиореспираторной выносливости является прямое измерение максимального потребления кислорода путём проведения кардиопульмонального нагрузочного тестирования (КПНТ). В связи с этим, мониторинг уровня лактата в крови наряду с уровнем пикового потребления кислорода по данным КПНТ можно эффективно использовать при планировании дальнейших научных исследований Поиск, отбор и анализ литературных источников по данной теме осуществлялся в научных базах CyberLeninka, eLibrary.ru, link.springer.com, frontiersin.org, pubmed.ncbi.nlm.nih.gov, Google Scholar и других, и был направлен на систематизацию современных доказательств, подтверждающих роль митохондриальной дисфункции как патогенетического механизма длительного COVID.

Ключевые слова: митохондрии, гликолиз, активные формы кислорода, аденозинтрифосфат, метаболическое перепрограммирование, длительный COVID, лактат, кардиореспираторная выносливость, кардиопульмональное нагрузочное тестирование

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Despite the end of the COVID-19 pandemic, many patients continue to experience adverse sequelae of the disease, including cardiometabolic disturbances. The spectrum of symptoms associated with long COVID is broad and heterogeneous, necessitating a deeper understanding of the underlying mechanisms. One of the proposed mechanisms contributing to long COVID is transient postviral mitochondrial dysfunction. It is hypothesized that SARS-CoV-2, either directly or indirectly via systemic inflammation, induces metabolic reprogramming of cells, leading to impaired oxidative phosphorylation, reduced ATP production, and increased generation of reactive oxygen species (ROS). Under conditions of metabolic reprogramming, cells preferentially rely on glycolysis for lactate production. Elevated blood lactate levels at low exercise intensity are indicative of mitochondrial dysfunction. Cardiorespiratory fitness is directly related to the integrated function of multiple physiological systems and is considered a reflection of overall health status. The most objective and accurate measure of cardiorespiratory fitness is the direct assessment of maximal oxygen uptake (VO₂max) using cardiopulmonary exercise testing (CPET). Accordingly, monitoring blood lactate levels in conjunction with peak oxygen consumption assessed by CPET may be effectively used in the design of future research studies. The search, selection, and analysis of relevant sources were conducted using scientific databases including cyberleninka.ru, elibrary.ru, link.springer.com, frontiersin.org, pubmed.ncbi.nlm.nih.gov, Google Scholar, and others, with the aim of systematizing current evidence supporting mitochondrial dysfunction as a key pathogenetic mechanism of long COVID.

Keywords: mitochondria, glycolysis, reactive oxygen species, adenosine triphosphate, metabolic reprogramming, long COVID, lactate, cardiorespiratory fitness, cardiopulmonary exercise testing

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Авторы

К.С. Авдеева*, Т.И. Петелина, А.В. Горбачевский, М.И. Бессонова

Тюменский кардиологический научный центр, Томский национальный исследовательский медицинский центр Российской академии наук, Томск, Россия
*avdeeva_03@mail.ru

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Ksenia S. Avdeeva*, Tatiana I. Petelina, Aleksandr V. Gorbachevskii, Marina I. Bessonova

Tyumen Cardiology Research Center, Tomsk National Research Medical Center of the Russian Academy of Sciences, Tomsk, Russia
*avdeeva_03@mail.ru

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