Key result
Hydrogen sulfide exerts protective effects against myocardial ischemia/reperfusion injury through antioxidant, anti-apoptotic, anti-inflammatory, and mitochondrial preservation mechanisms.
Why the study?
Many mechanisms have recently been proposed and verified regarding the cardioprotective effects of hydrogen sulfide, motivating a review of its role against myocardial ischemia/reperfusion injury.
Does hydrogen sulfide provide protection against myocardial ischemia/reperfusion injury in experimental models?
Does hydrogen sulfide provide protection against myocardial ischemia/reperfusion injury in experimental models?
Hydrogen sulfide demonstrates significant cardioprotective potential against ischemia/reperfusion injury in preclinical models through multiple molecular pathways, highlighting its potential as a future therapeutic target.
H2S-mediated cardiovascular protection is hypothesis-generating; leaves open prospective trials before any clinical consideration.
Hydrogen sulfide (H 2 S) is recognized to be a novel mediator after carbon monoxide and nitric oxide in the organism. It can be produced in various mammalian tissues and exert many physiological effects in many systems including the cardiovascular system. A great amount of recent studies have demonstrated that endogenous H 2 S and exogenous H 2 S-releasing compounds (such as NaHS, Na 2 S, and GYY4137) provide protection in many cardiovascular diseases, such as ischemia/reperfusion injury, heart failure, cardiac hypertrophy, and atherosclerosis. In recent years, many mechanisms have been proposed and verified the protective role exhibited by H 2 S against myocardial ischemia/reperfusion injury, and this review is to demonstrate the protective role of exogenous and endogenous H 2 S on myocardial ischemia/reperfusion injury.
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Zhang et al. (2021) conducted a review in Myocardial ischemia/reperfusion injury. Hydrogen sulfide (H2S) was evaluated. Hydrogen sulfide exerts protective effects against myocardial ischemia/reperfusion injury through antioxidant, anti-apoptotic, anti-inflammatory, and mitochondrial preservation mechanisms.
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