Authors
G V Grigorenko, V V Tsurko
Published in
Terapevticheskii arkhiv. Volume 98. Issue 5. Pages 320-324. Jun 13, 2026. Epub Jun 13, 2026.
Abstract
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.
PMID:
42378525
Bibliographic data and abstract were imported from PubMed on 01 Jul 2026.
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