Besides its well-known protective effect on cardiac hypertrophy, remodeling and fibrosis, we could demonstrate that DOX was able to decrease the ROS-induced mitochondrial fragmentation and depolarisation on H9C2 cardiomyocytes, and beneficially modulated the steady state level of OPA-1, Mfn-2 and the phosphorylation of Drp-1 in our postinfarction heart failure model. The gene discussed is MFN2; the disease is heart failure.