Skip to main content
Fig. 13 | Particle and Fibre Toxicology

Fig. 13

From: Osteopontin enhances multi-walled carbon nanotube-triggered lung fibrosis by promoting TGF-β1 activation and myofibroblast differentiation

Fig. 13

A working model of induced lung fibrosis through OPN. Pulmonary exposure to MWCNTs induces the expression and secretion of OPN in the lungs. Increased OPN stimulates the expression and activation of TGF-β1, and promotes the activation of Smad-dependent TGF-β1 signaling, indicated by phosphorylation and nuclear translocation of Smad2/3, in fibroblasts and myofibroblasts. The activation of Smad-dependent TGF-β1 signaling in fibroblasts induces fibroblast-to-myofibroblast differentiation; and the activation of Smad-dependent TGF-β1 signaling in myofibroblasts results in excessive production and deposition of ECM proteins in lung tissues. Through this signaling cascade, OPN plays an important role in the initiation and progression of MWCNT-induced lung fibrosis

Back to article page

Particle and Fibre Toxicology

ISSN: 1743-8977

Contact us