Sirt3 Impairment and SOD2 Hyperacetylation in Vascular Oxidative Stress and Hypertension.

ABSTRACT:

Rationale

Clinical studies have shown that Sirt3 (Sirtuin 3) expression declines by 40% by 65 years of age paralleling the increased incidence of hypertension and metabolic conditions further inactivate Sirt3 because of increased NADH (nicotinamide adenine dinucleotide, reduced form) and acetyl-CoA levels. Sirt3 impairment reduces the activity of a key mitochondrial antioxidant enzyme, superoxide dismutase 2 (SOD2) because of hyperacetylation.

Objective

In this study, we examined whether the loss of Sirt3 activity increases vascular oxidative stress because of SOD2 hyperacetylation and promotes endothelial dysfunction and hypertension.

Methods and results

Hypertension was markedly increased in Sirt3-knockout (Sirt3^-/-) and SOD2-depleted (SOD2

SUBMITTER: Dikalova AE 

PROVIDER: S-EPMC5562527 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature