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During acute myocardial infarction,endoplasmic reticulum(ER)stress-induced autophagy and apoptosis have been shown as important pathogeneses of myocardial reconstruction.Importantly,hydrogen sulfide(H2S),as a third endogenous gas signaling molecule,exerts strong cytopro-tective effect on anti-ER stress,autophagy regulation and antiapoptosis.Here,we showed that H2S treatment inhibits apoptosis by regulating ER stress-autophagy axis and improves myocar-dial reconstruction after acute myocardial infarction.We found that H2S intervention improved left ventricle function,reduced glycogen deposition in myocardial tissue mesenchyme,and inhibited apoptosis.Moreover,the expressions of fibrosis indicators(Col3a1 and Colla2),ER stress-related proteins(CHOP and BIP/ERP78),autophagy-related proteins(Beclin and ATG5),apoptosis pro-tein(Bax),as well as fibrosis protein Col4a3bp were all decreased after treatment with H2S.H2S administration also maintained MMP/TIMP balance.Mechanistically,H2S activated the PI3K/AKT signaling pathway.In addition,H2S treatment also reduced the expressions of ER stress-related proteins,autophagy-related proteins,and apoptins in in vitro experiments.Interestingly,activation of ER stress-autophagy axis could reverse the inhibitory efect of H2S on myocardial apopto-sis.Altogether,these results suggested that exogenous H2S suppresses myocardial apoptosis by blocking ER stress-autophagy axis,which in turn reverses cardiac remodeling after myocardial infarction.