Previous studies have shown that lysine-specific demethylase 3A (KDM3A) is involved in myocardial ischemia‒reperfusion injury after MI by regulating key signaling pathways such as inflammation, apoptosis, and oxidative stress, and subsequent studies further confirmed that H19 regulates the expression of KDM3A through competitive binding to miR-22-3p, thus improving myocardial injury induced by MI [17]. Here, H19 is linked to myocardial infarction.