Hydrogen sulfide plays an important role by regulating endoplasmic reticulum stress in myocardial diseases

Endoplasmic reticulum (ER) is an important organelle for protein translation, folding and translocation, as well as the post-translational modification and assembly of newly synthesized secreted proteins. When the excessive accumulation of misfolded and/or unfolded proteins exceeds the processing capacity of ER, ER stress is triggered. The integrated intracellular signal cascade, namely the unfolded protein response, is induced to avoid ER stress. ER stress is involved in many pathological and physiological processes including myocardial diseases. For a long time, hydrogen sulfide (H(2)S) has been considered as a toxic gas with the smell of rotten eggs. However, more and more evidences indicate that H(2)S is an important gas signal molecule after nitric oxide and carbon monoxide, and regulates a variety of physiological and pathological processes in mammals. In recent years, increasing studies have focused on the regulatory effects of H(2)S on ER stress in myocardial diseases, however, the mechanism is not very clear. Therefore, this review focuses on the role of H(2)S regulation of ER stress in myocardial diseases, and deeply analyzes the relevant mechanisms so as to lay the foundation for the future researches.