Hydrogen Sulfide Attenuates Angiotensin II-Induced Cardiac Fibroblast Proliferation and Transverse Aortic Constriction-Induced Myocardial Fibrosis through Oxidative Stress Inhibition via Sirtuin 3

Figure 9

Illustration of the mechanism of protective effects on myocardial fibrosis by H₂S. H₂S enhanced SIRT3 transcription, decreased the DRP1 level, ameliorated mitochondrial membrane rupture, suppressed oxidative stress, and alleviated Ang II-induced cardiac fibroblast proliferation and TAC-induced myocardial fibrosis. However, these protective effects of H₂S were unavailable if SIRT3 was silenced in cells or deficient in mice. It suggested that H₂S attenuated myocardial fibrosis through oxidative stress inhibition via a SIRT3-dependent manner.