Inhibition of Mitochondrial Oxidative Damage Improves Reendothelialization Capacity of Endothelial Progenitor Cell via SIRT3 (Sirtuin 3)-Enhanced SOD2 (Superoxide Dismutase) Deacetylation in Hypertension.

Conclusions- The present study demonstrated for the first time that mitochondrial oxidative damage because of deficient SIRT3/SOD2 signaling contributes to the decline in reendothelialization capacity of EPCs in hypertension. Maintenance of mitochondrial redox homeostasis in EPCs may be a novel therapeutic target for endothelial injury.
PMID: 31189433 [PubMed - as supplied by publisher]

Source: Arteriosclerosis, Thrombosis and Vascular Biology - June 12, 2019 Category: Cardiology Authors: He J, Liu X, Su C, Wu F, Sun J, Zhang J, Yang X, Zhang C, Zhou Z, Zhang X, Lin X, Tao J Tags: Arterioscler Thromb Vasc Biol Source Type: research