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LIVER FIBROSIS is the common response to chronic liver injury and is due abnormal accumulation of extracellular matrix (ECM). In response to injury, activated hepatic stellate cells (HSCs) proliferate and produce excess amount of ECM in response to inflammatory cytokines and growth factors. Among these mediators, transforming growth factor-β (TGF-β) is the major pro-fibrogenic cytokine, up-regulating the expression of α-smooth muscle actin (α-SMA) and type 1 collagen α (COL1A) synthesis via Smad signaling pathway, while platelet-derived growth factor (PDGF) is a potent mitogen for HSCs via activation of extracellular signal-regulated protein kinase/mitogen-activated protein kinase and phosphoinositide-3-kinase pathways. Currently, inhibition of TGF-β and/or PDGF signaling pathways is considered as a promising anti-fibrotic strategy.

american journal of physiology. cell physiology

<i>Novel insight into a platelet-derived growth factor-C/Smad3 axis in liver fibrosis</i>. Focus on “Role of Smad3 in platelet-derived growth factor-C-induced liver fibrosis”

Novel insight into a platelet-derived growth factor-C/Smad3 axis in liver fibrosis. Focus on “Role of Smad3 in platelet-derived growth factor-C-induced liver fibrosis”