However, treatment with the ETAR antagonist attenuated myocyte apoptosis in cultured cells [161] and in animal models of MI [162], I/R [163], or doxorubicin-induced cardiomyopathy [164], indicating that endogenous endothelin-1 and ETAR are proapoptotic under these conditions. The gene discussed is EDNRA; the disease is myocardial infarction.