The study identifies Sirt3 impairment and subsequent SOD2 inactivation as a mechanistic contributor to vascular oxidative stress and hypertension.
Sirt3-SOD2 pathway merits preclinical hypertension studies; animal data leave human therapeutic relevance open.
Our data suggest that diminished Sirt3 expression and redox inactivation of Sirt3 lead to SOD2 inactivation and contributes to the pathogenesis of hypertension.
No takes yet. Share an insight, caveat, or question.
Dikalova et al. (2017) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: