The study identifies Sirt3 impairment and subsequent SOD2 inactivation as a mechanistic contributor to vascular oxidative stress and hypertension.
Our data suggest that diminished Sirt3 expression and redox inactivation of Sirt3 lead to SOD2 inactivation and contributes to the pathogenesis of hypertension.
Dikalova et al. (2017) studied this question.