Recently, TRPV4-induced intracellular Ca2+ overload was shown to mediate mechanical stress-induced damage (O’Neil and Heller, 2005) and participate in pathophysiological processes, such as vasoconstriction, edema, and apoptosis, eventually leading to pathological changes, such as pulmonary vascular endothelial injury (Jian et al., 2008) and myocardial ischemia (Dong et al., 2017). This evidence concerns the gene TRPV4 and myocardial ischemia.