内质网应激（ERS）－自噬通路对缺血再灌注（IR）后心肌细胞存亡发挥着枢纽性作用，而且ERS相关分子表达或活化可被气体信号分子硫化氢调节。我们前期的研究证实硫化氢还能激活心肌mTOR，并抑制自噬相关基因及标志蛋白的异常增加。提示硫化氢可能通过ERS－mTOR通路，调控细胞自噬的发生。本项目首先在整体心肌IR损伤模型上，研究硫化氢对ERS－自噬的影响；并在心肌细胞缺氧/复氧模型基础上，应用相关通路抑制剂，进一步研究其对ERS－mTOR－自噬的调控，重点探讨沉默或过表达ERS相关基因（PERK、IRE1、ATF6、CHOP等）对硫化氢抑制心肌细胞自噬作用的影响，明确其是否可通过ERS-mTOR通路，调控Atg家族表达，减少心肌细胞自噬发生，发挥其心脏保护作用。本研究有助于揭示硫化氢调控自噬相关基因表达及抑制心肌细胞自噬的可能信号转导机制，为硫化氢相关药物研发及临床心肌保护提供新的思路。

Endoplasmic reticulum stress (ERS)-autophagy pathway is reported crucial for myocardial cells survival after ischemia / reperfusion (IR) injury. Hydrogen sulfide (H2S) could modulate the expression and activation of ERS related molecule. Our preliminary data demonstrated that H2S could activate myocyte mammalian target of rapamycin (mTOR) and inhibit unusual overexpression of autophagy-related gene (Atg) and autophagy marker protein. We hypothesised that ERS-mTOR mediated cardiac protective effect of H2S through down-regulating autophagy. This study is designed to investigate the effect of H2S on ERS-autophagy and its possible molecular mechanism on the IR injury model as well as on the hypoxia / reoxygenation cultured myocyte model. We try to identify how H2S regulates ERS-mTOR-autophagy by using the suppressors related and put emphasis on how H2S inhibits myocardial autophagy by knockdown and over expression of ERS related genes (PERK, IRE1, ATF6, CHOP) in cultured myocytes. The aim is to elucidate whether H2S coud regulate Atg family and inhibit myocyte autophagy by attenuating ERS to conduct mycardial protective effect. Results gained from this study will light the probably mechanism of H2S regulating myocyte ERS-induced autophagy. It will provide new vision and help with the development of H2S simulated medication and novel therapies for clinical cardioprotection.