Skip to main content
. Author manuscript; available in PMC: 2014 Jan 23.
Published in final edited form as: Annu Rev Pathol. 2013 Jan 24;8:161–187. doi: 10.1146/annurev-pathol-020712-163942

Figure 5.

Figure 5

Hypothetical model of asbestos-induced pulmonary fibrosis. Asbestos elicits a macrophage response to phagocytize and clear the fibers, but this response results in reactive oxygen species (ROS) production by a Rac1-dependent mechanism as well as the release of cytokines and growth factors. Asbestos-induced alveolar macrophage (AM) and alveolar epithelial cell (AEC) mitochondrial ROS production promotes AEC apoptosis that may be important for myofibroblast differentiation, collagen deposition by myofibroblasts, and ultimately pulmonary fibrosis. Abbreviations: PDGF, platelet-derived growth factor; IL, interleukin; Rac1, Ras-related C3 botulinum toxin substrate 1; TGF, transforming growth factor; TNF, tumor necrosis factor.