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. Author manuscript; available in PMC: 2013 Jun 7.
Published in final edited form as: Kidney Int. 2011 Feb 9;79(9):944–956. doi: 10.1038/ki.2010.516

Figure 1. Proposed origin(s) of interstitial myofibroblasts during fibrosis.

Figure 1

Proposed origin(s) of interstitial myofibroblasts during fibrosis. Myofibroblasts responsible for interstitial expansion and structural damage during progressive organ injury have been proposed to be derived from one or more sources: (1) activation of resident fibroblasts or pericytes, (2) infiltration of circulating bone marrow-derived fibrocytes, (3) expansion of perivascular adventitial fibroblasts, (4) endothelial–mesenchymal (EndoMT) transition, and/or (5) epithelial-to-mesenchymal transition (EMT). Transforming growth factor-beta (TGF-β) released via paracrine or autocrine pathways induces myofibroblast differentiation expressed by the acquisition of an alpha-smooth muscle actin (α-SMA) phenotype and consequent synthesis of mesenchymal matrix proteins collagen type I (Col I), collagen type III (Col III), and fibronectin EIIIA (FN). Nox NAD(P)H oxidase (Nox4)-derived reactive oxygen species (ROS) have a central role in TGF-β signaling of myofibroblast differentiation.