The roles of hydrogen sulfide in renal physiology and disease states

Hydrogen sulfide (H₂S), an endogenous gaseous signaling transmitter, has gained recognition for its physiological effects. In this review, we aim to summarize and discuss existing studies about the roles of H₂S in renal functions and renal disease as well as the underlying mechanisms. H₂S is mainly produced by four pathways, and the kidneys are major H₂S-producing organs. Previous studies have shown that H₂S can impact multiple signaling pathways via sulfhydration. In renal physiology, H₂S promotes kidney excretion, regulates renin release and increases ATP production as a sensor for oxygen. H₂S is also involved in the development of kidney disease. H₂S has been implicated in renal ischemia/reperfusion and cisplatin-and sepsis-induced kidney disease. In chronic kidney diseases, especially diabetic nephropathy, hypertensive nephropathy and obstructive kidney disease, H₂S attenuates disease progression by regulating oxidative stress, inflammation and the renin-angiotensin-aldosterone system. Despite accumulating evidence from experimental studies suggesting the potential roles of H₂S donors in the treatment of kidney disease, these results need further clinical translation. Therefore, expanding the understanding of H₂S can not only promote our further understanding of renal physiology but also lay a foundation for transforming H₂S into a target for specific kidney diseases.