Abstract:Background
Fibroblast/myofibroblast transdifferentiation following acute cardiac injury (MI) is a major mechanism of scar formation and adverse remodeling regulated by TGFβ/SMAD3 signaling. Myofibroblasts represent phenotypically modulated cells characterized by α-smooth muscle actin (α-SMA) and constitute the main source of extracellular matrix proteins such as collagen type I in the healing infarct wound. Moreover, the recruitment of a specific monocyte/macrophages subset (Ly6Chigh and Ly6C… Show more
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