This study investigates the cardioprotective effects of hydrogen sulfide (H₂S) in a murine model of myocardial ischemia-reperfusion (MI-R). The researchers found that administering H₂S during reperfusion significantly reduced infarct size and preserved left ventricular (LV) function. This protection is associated with reduced myocardial inflammation, preserved mitochondrial function, and decreased cardiomyocyte apoptosis. Additionally, overexpression of cystathionine γ-lyase (CGL) in cardiac-specific transgenic mice increased H₂S production, further limiting the extent of MI-R injury. The findings suggest that H₂S may be a valuable therapeutic agent for treating acute myocardial infarction, either by direct administration or by modulating endogenous H₂S production.This study investigates the cardioprotective effects of hydrogen sulfide (H₂S) in a murine model of myocardial ischemia-reperfusion (MI-R). The researchers found that administering H₂S during reperfusion significantly reduced infarct size and preserved left ventricular (LV) function. This protection is associated with reduced myocardial inflammation, preserved mitochondrial function, and decreased cardiomyocyte apoptosis. Additionally, overexpression of cystathionine γ-lyase (CGL) in cardiac-specific transgenic mice increased H₂S production, further limiting the extent of MI-R injury. The findings suggest that H₂S may be a valuable therapeutic agent for treating acute myocardial infarction, either by direct administration or by modulating endogenous H₂S production.