Authors
Siyun Kim, Sung Gi Noh, Minje Ji, Kai Chen, George A Kuchel, Iman M Al-Naggar, Oh Sung Kwon
Published in
GeroScience. Sep 28, 2026. Epub Sep 28, 2026.
Abstract
Aging is an inevitable and progressive physiological process marked by a decline in cellular function, accumulation of somatic mutations, decreased ability to maintain homeostasis, and increased tissue and organ dysfunction. These changes contribute to the onset and progression of various age-related diseases. Accumulation of reactive oxygen species (ROS) has been identified as a key mediator of the aging process. Mitochondria, the primary producers of ROS, accumulate defects with aging, leading to increased mitochondrial oxidative stress. These defective mitochondria are both a source and a target of oxidative stress, creating a vicious cycle that accelerates aging and the progression of age-related diseases. Consequently, targeting mitochondria represents a promising therapeutic approach to prevent aging-related physiological dysfunction. MitoQ, a mitochondria-targeted antioxidant, has been extensively studied due to its ability to effectively scavenge mitochondria-derived ROS, owing to its lipophilic cation properties. This review explores the effects of MitoQ on aging-associated physiological dysfunction, specifically exploring its impact on cardiovascular, neuronal, and skeletal muscle functions. By addressing the central role of mitochondrial oxidative stress, we propose that MitoQ represents a promising strategy to counteract aging-associated physiological dysfunction.
PMID:
42806210
Bibliographic data and abstract were imported from PubMed on 18 Oct 2026.
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