In our meta-analysis, TGFß1 and one of its signal transducers (SMAD3) were consistently upregulated two to fourfold in the hearts of animals with anthracycline-induced cardiomyopathy from 0.8 to 4.7 human equivalent years after anthracycline administration, suggesting pro-fibrotic signaling is present at both early and late stages. Here, SMAD3 is linked to cardiomyopathy.