H2S-mediated blockage of protein acetylation and oxidative stress attenuates lipid overload-induced cardiac senescence

Hydrogen sulphide (H2S), a newly identified gasotransmitter, can be endogenously produced by cystathionine gamma-lyase (CSE) in the cardiovascular system. This study investigated role of CSE/H2S system on lipid overload-induced lipotoxicity and cardiac senescence. Lipid overload rat cardiomyocyte cells (H9C2) promoted intracellular accumulation lipid, oxidative stress, mitochondrial dysfunctions, peroxidation inhibited cell viability, all which could reversed exogenously applied H2S. Further data revealed that H2S protected H9C2 from senescence altering expressions metabolism-related genes inhibiting cellular acetyl-CoA global protein acetylation. Enhancement acetylation abolished protective In vivo, knockout CSE gene strengthened accumulation, acetylation, ageing high fat diet-fed mice. Taken together, is capable maintaining homeostasis heart under overload.