ADAM17 and cardiomyopathy: These results suggested that ADAM17 deficiency abolished TAK1 and MAPKs pathway activation induced by doxorubicin, while ADAM17 overexpression promoted cardiomyocyte apoptosis in doxorubicin-induced cardiomyopathy by activating TAK1, JNK, P38 MAPK and ERK pathway in vivo and in vitro.