More recently, this redox crosstalk concept was extended; in AT-II-induced hypertension, NOX-2 activation triggers Sirt3 S-glutathionylation leading to acetylation of vascular SOD2 and reduced SOD2 activity, all of which resulted in elevated mitochondrial superoxide, diminished endothelial nitric oxide bioavailability, and aggravation of hypertension [107, 108]. This evidence concerns the gene SOD2 and hypertensive disorder.