As a classical pathogenic mechanism of a variety of cardiovascular diseases, stress-induced cardiomyocyte apoptosis has been proved to be related to the reduction of anti-apoptotic Bcl-2 and the increase in pro-apoptotic Bax and cleaved caspase-3 via activing the Wnt/β-catenin pathway [44]. Here, CASP3 is linked to cardiovascular disorder.