NAD(P)H Oxidase 4 Mediates Transforming Growth Factor-β1–Induced Differentiation of Cardiac Fibroblasts Into Myofibroblasts

By Ioan Cucoranu, R. Clempus, A. Dikalova, Patrick J. Phelan, S. Ariyan, S. Dikalov, D. Sorescu. Circulation Research, 2005

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NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart (2010, background): “However, Nox4 expressed in cardiac fibroblasts may also play an important role in mediating cardiac fibrosis by stimulating myofibroblast differentiation (27).”
The role of TGF-β Signaling in Myocardial Infarction and Cardiac Remodeling (2007, background): “TGF-β markedly enhances collagen types I and III synthesis [57], decreases collagenase expression, increases TIMP-1 synthesis [58], upregulates integrin expression and induces acquisition of the myofibroblastic phenotype in isolated cardiac fibroblasts [ 59 ].”
The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology. (2007, background): “Heart (55, 143) (79, 143, 372, 454, 963) (120, 143, 813) Cardiomyocytes (457) (488, 537, 601, 963) (120) (626) (457) (626) Developing cardiomyocytes (536) (536) (536) (790) Endothelium (537) Fibroblast (176) (176) (176) Phagocytes (560)”
Nox proteins in signal transduction (2009, neutral): “[169], keratinocytes [170], osteoclasts [16], neurons [171], and hepatocytes [172].”
NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential (2020, background): “Under the acceleration of TGF-β1, Nox4 mRNA is significantly upregulated and mediates the transformation of fibroblasts into myofibroblasts by activating TGFβ1-Smad2/3 signaling, which leads to cardiac fibrosis.(586,587)”