SMAD2 and myocardial infarction: Their findings revealed that both aerobic andresistance exercise training up-regulated the expression of fibroblast growthfactor 21 protein, inactivated the TGF-β1-mothers against DPP homolog 2/3(Smad2/3)-matrix metalloproteinase 2/9 (MMP2/9) signalingpathway, reduced collagen production, alleviated cardiac fibrosis, and ultimatelyimproved cardiac function in MI mice.