Terapevticheskii arkhivTerapevticheskii arkhivТерапевтический архив0040-36602309-5342LLC Obyedinennaya Redaktsiya70005910.26442/00403660.2026.05.203610ReviewsОбзорыReview ArticleUric acid and mitochondrial dysfunction: a reviewМочевая кислота и митохондриальная дисфункция: обзорная статьяhttps://orcid.org/0009-0000-0886-2359GrigorenkoGavriil V.ГригоренкоГавриил Викторович
Russian Federation

студент VI курса Института клинической медицины

gvgrigoren@gmail.comhttps://orcid.org/0000-0001-8040-3704TsurkoVladimir V.ЦуркоВладимир Викторович
Russian Federation

д-р мед. наук, проф. Института клинической медицины

gvgrigoren@gmail.comPirogov Russian National Research Medical University (Pirogov University)ФГАОУ ВО «Российский национальный исследовательский медицинский университет им. Н.И. Пирогова» Минздрава России (Пироговский Университет)13062026985Issues of rheumatologyВопросы ревматологии3203243012202520022026Copyright ©; 2026, Consilium MedicumCopyright ©; 2026, ООО "Консилиум Медикум"2026Consilium MedicumООО "Консилиум Медикум"https://creativecommons.org/licenses/by-nc-sa/4.0https://ter-arkhiv.ru/0040-3660/article/view/700059

The relationship between hyperuricemia and mitochondrial dysfunction remains poorly described in literature, despite its important clinical significance. The aim of this review is to identify the causes and mechanisms of uric acid's influence on the development of mitochondrial dysfunction. This review presents a comprehensive analysis of the pathogenetic relationship between uric acid (UA) and mitochondrial dysfunction as an evolutionarily formed process aimed at maintaining cellular energy homeostasis in conditions of energy deficiency, but modified into a pathological process in modern conditions of over-nutrition. The important role of the metabolism of fructose and its metabolite, UA, in the regulation of the energy balance of the cell is analyzed. The mechanisms of increased oxidative stress caused by UA and their effect on mitochondrial function have been determined. The important role of AMP-activated protein kinase (AMPK), a key regulator of cellular homeostasis, is analyzed, the inhibition of which by UA leads to mitochondrial dysfunction.

Взаимосвязь гиперурикемии и митохондриальной дисфункции остается недостаточно изученной в литературе, несмотря на ее важное клиническое значение. Цель обзора состоит в выявлении причин и механизмов влияния мочевой кислоты (МК) на развитие митохондриальной дисфункции. В статье представлен комплексный анализ патогенетической взаимосвязи между МК и митохондриальной дисфункцией как об эволюционно сформированном процессе, направленном на поддержание энергетического гомеостаза клетки в условиях энергетического дефицита, но видоизмененном в современных условиях избыточного питания в патологический процесс. Проанализирована важная роль метаболизма фруктозы и его метаболита – МК – в регуляции энергетического баланса клетки. Определены механизмы усиления оксидативного стресса, вызываемого МК, и их влияние на функцию митохондрий. Проанализирована важная роль ключевого регулятора клеточного гомеостаза – аденозинмонофосфат-активируемой протеинкиназы (AMPK), ингибирование которого МК приводит к митохондриальной дисфункции.

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