Smad Cofactors/Corepressors in the Fibrosed Post-MI Heart: Possible Therapeutic Targets

摘要: Several axioms that govern our understanding of the pathogenesis post-MI congestive heart failure have recently been questioned or revisited in lieu relative flood new data addressing role cardiac non-myocytes this disease state. Among these is assumption matrix necessarily serves a secondary to initial progressive dysfunction myocytes. It now well established remodeling interstitium separate and distinct contributor progression failure, turnover extracellular rapid enough be relevant disease. As fibroblasts myofibroblasts are main source regulate wound healing, study stimulating ligands their signaling pathways may reveal novel sites for therapeutic intervention. This chapter provides background on interstitial components as providing support argument need address post-receptor classical TGF-s regulation (myo)fibroblast function, with an emphasis Smad proteins cofactors/corepressors.