TGFB1 and myocardial infarction: Suppression and resolution of the inflammation, which are partly mediated by anti-inflammatory and pro-fibrotic cytokines (such as IL-10 and TGF-β1), are critical for optimal wound healing; dysregulation of them, in combination with overactive myocardial fibrosis, contribute to the pathogenesis of adverse left ventricular (LV) remodeling and eventually heart failure (HF) after MI [47].