Treatment of wild type mice with SA13353 led to improved cardiac function, while capsazepine administered to ALDH2TG mice abrogated increased contractility evoked by ALDH2 overexpression, respectively, which indicates that cardioprotection induced by ALDH2 overexpression against doxorubicin-induced heart failure is mediated at least partially by TRPV1. Here, ALDH2 is linked to heart failure.