Smad3 Signaling Critically Regulates Fibroblast Phenotype and Function in Healing Myocardial Infarction

Abstract

Disruption of Smad3 results in infiltration of the infarct with abundant hypofunctional fibroblasts that exhibit impaired myofibroblast transdifferentiation, reduced migratory potential, and suppressed expression of fibrosis-associated genes.