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 (H2S) has been considered as a toxic gas with the smell of rotten eggs. However, more and more evidences indicate that H2S 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 H2S on ER stress in myocardial diseases, however, the mechanism is not very clear. Therefore, this review focuses on the role of H2S regulation of ER stress in myocardial diseases, and deeply analyzes the relevant mechanisms so as to lay the foundation for the future researches.

Automated summary

Endoplasmic reticulum (ER) plays a critical role in protein synthesis and processing. When ER is overloaded with misfolded proteins, ER stress is triggered. Hydrogen sulfide (H2S) has been recognized as an important gas signal molecule, with regulatory effects on various physiological and pathological processes. This review focuses on the role of H2S in regulating ER stress in myocardial diseases, aiming to provide a better understanding of its mechanisms.