Spatiotemporal regulation of hydrogen sulfide signaling in the kidney

Hydrogen sulfide (H2S) has long been recognized as a putrid, toxic gas. However, result of intensive biochemical research in the past two decades, H2S is now considered to be third gasotransmitter alongside nitric oxide (NO) and carbon monoxide (CO) mammalian systems. H2S-producing enzymes are expressed all organs, playing an important role their physiology. In kidney, critical regulator vascular cellular function, although mechanisms that affect (sub)cellular levels not precisely understood. modulates systemic renal blood flow, glomerular filtration rate renin-angiotensin axis through direct inhibition synthesis. Further, affects function by modulating protein activity via post-translational modification: process termed persulfidation. Persulfidation activity, localization protein-protein interactions. Additionally, acute kidney injury (AKI) due mitochondrial dysfunction, which occurs during hypoxia or ischemia-reperfusion (IR), attenuated H2S. enhances ATP production, prevents damage free radicals regulates endoplasmic reticulum stress IR. this review, we discuss current insights regulation anabolism, retention catabolism, with relevance spatiotemporal levels. Together, versatile pleiotropic effects on offers protection against AKI. Unraveling modulate signaling only expands fundamental insight functional mediated H2S, but can also provide novel therapeutic targets prevent hypoxic ischemic injury.