The cardioprotective effects of hydrogen sulfide by targeting endoplasmic reticulum stress and the Nrf2 signaling pathway: A review

Cardiac diseases are emerging due to lifestyle, urbanization, and the accelerated aging process. Oxidative stress has been associated with cardiac injury progression through interference with antioxidant strategies and endoplasmic reticulum (ER) function. Hydrogen sulfide (H2S) is generated endogenously from l-cysteine in various tissues including heart tissue. Pharmacological evaluation of H2S has suggested a potential role for H2S against diabetic cardiomyopathy, ischemia/reperfusion injury, myocardial infarction, and cardiotoxicity. Nuclear factor E2-related factor 2 (Nrf2) activity is crucial for cell survival in response to oxidative stress. H2S up-regulates Nrf2 expression and its related signaling pathway in myocytes. H2S also suppresses the expression and activity of ER stress-related proteins. H2S has been reported to improve various cardiac conditions through antioxidant and anti-ER stress-related activities.

Automated summary

Cardiac diseases are on the rise due to lifestyle changes, urbanization, and aging, with oxidative stress playing a key role in cardiac injury progression. Hydrogen sulfide (H2S) has shown potential in improving various cardiac conditions through antioxidant and anti-ER stress-related activities, by regulating Nrf2 expression and its signaling pathway in myocytes.