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Fibrosis is defined as an excessive accumulation of extracellular matrix components that lead to the destruction of organ architecture and impairment of organ function. Moreover, fibrosis is an intricate process attributable to a variety of interlaced fibrogenic signals and intrinsic mechanisms of activation of myofibroblasts. Being the dominant matrix-producing cells in organ fibrosis, myofibroblasts may be differentiated from various types of precursor cells. Identification of the signal pathways that play a key role in the pathogenesis of fibrotic diseases may suggest potential therapeutic targets. Here, we emphasize several intracellular signaling pathways that control the activation of myofibroblasts and matrix production.
Keywords:
Fibrosis; Mitogen-activated protein kinase; Phosphoinositide 3 kinase; Smad; Sonic hedgehog; Wnt/β-catenin.
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