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Myofibroblast differentiation suppression refers to pharmacological or genetic interventions aimed at preventing or reversing the conversion of precursor cells (typically fibroblasts) into myofibroblasts. Myofibroblasts are characterized by the expression of markers such as α-smooth muscle actin and contribute to tissue fibrosis through extracellular matrix production and tissue contractility. This process is often driven by TGF-β1 and involves multiple signaling pathways (MAPK, AMPK, Hedgehog, VEGF, NOX4-derived ROS, and others). Inhibition of myofibroblast differentiation is being actively researched as a therapeutic concept to treat fibrotic diseases and reduce pathological tissue remodeling, but it is not a specific single molecular target, receptor, enzyme, or protein.
Inhibition of TGF-β1–induced signaling; Suppression of Hedgehog (Hh) and VEGF signaling; AMPK activation; Inhibition of mTOR signaling; Inhibition of mitochondrial oxidative phosphorylation (OXPHOS)
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