Does smad3 signaling critically regulate fibroblast phenotype and function in healing myocardial infarction?
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.
VEC expression was maintained during CI; however, it reduced early after reperfusion after 6 hours of CI, correlating with severe intraalveolar edema. db-cAMP/NTG additive to the preservation solution contributed to the maintenance of VEC expression after reperfusion.