Figure 1.

Alterations in normal wound healing processes promote the development of pulmonary fibrosis. (A) After radiation injury epithelial cells release inflammatory mediators, triggering platelet aggregation and inflammatory cell recruitment and activation. (B) Pro-fibrotic and inflammatory cytokines released by recruited immune cells, such as macrophages and lymphocytes, promote the recruitment and differentiation of resident fibroblasts and circulating fibrocytes into ECM-secreting myofibroblasts. Fibroblasts and myofibroblasts may also originate from epithelial cells that have gone through the EMT process. (C) Activated myofibroblasts remodel ECM, actively promoting tissue repair by epithelial and endothelial cells and restoring lung function. (D) Disregulation of wound healing process and persisted inflammatory environment promote lung tissue fibrosis [29,30,31,32,33,34,35,36,37,38].