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Mitochondria-targeted antioxidant (MitoQ) ameliorates age-related arterial endothelial dysfunction in mice.

Age-related arterial endothelial dysfunction, a key antecedent to the development of cardiovascular diseases (CVD), is largely due to a reduction in nitric oxide (NO) bioavailability as a consequence of oxidative stress. Mitochondria are a major source and target of vascular oxidative stress when dysregulated. Mitochondrial dysregulation is associated with primary aging, but its role in age-related endothelial dysfunction is unknown. Our aim was to determine the efficacy of a mitochondria-targeted antioxidant, MitoQ, for ameliorating vascular endothelial dysfunction in old mice. The improvements in endothelial function with MitoQ supplementation were associated with normalization of age-related increases in total and mitochondria-derived arterial superoxide production and oxidative stress (nitrotyrosine abundance), as well as increases in markers of vascular mitochondrial health, including antioxidant status. MitoQ also reversed the age-related increase in endothelial susceptibility to acute mitochondrial damage (rotenone-induced impairment in EDD). Our results suggest that mitochondria-derived oxidative stress is an important mechanism underlying the development of endothelial dysfunction with primary aging. Mitochondria-targeted antioxidants such as MitoQ represent a promising, novel strategy for preserving vascular endothelial function with advancing age and preventing age-related CVD. (more)

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