SMAD3 and myocardial infarction: Fibroblast-specific deletion of Smad3 paradoxically led to unrestrained fibroblast proliferation, impaired scar remodeling, reduced collagen synthesis, and perturbed alignment of myofibroblasts after myocardial infarction by suppressing integrin-nicotinamide adenine dinucleotide phosphate oxidase-2 (NOX-2) signaling.