Fig. 9

Schematic diagram showing the mechanisms by which MCPIP1 in macrophages mediates silica-induced pulmonary fibrosis. MCPIP1 expression was increased in macrophages exposed to SiO2, leading to the subsequent enhancement of p53 expression. The interaction between MCPIP1 and p53 may be involved in the regulation of gene transcription and may enhance Bax expression, thereby promoting autophagic and apoptotic processes. Enhanced autophagy further stimulated macrophage apoptosis and activation, which resulted in overproduction of pro-fibrogenic cytokines by macrophages. Fibroblasts responding to these cytokines differentiated into myofibroblasts, which showed enhanced proliferation and migration capacities as well as increased collagen synthesis