Cytoprotective Strategy Against Pulmonary Fibrosis

Pulmonary fibrosis is a common response to injuries to the lung. Although there are various initiating factors or causes, the terminal stages are characterized by proliferation and progressive accumulation of connective tissue replacing normal functional parenchyma. The pathogenesis of pulmonary fibrosis includes endothelial and epithelial cell injury, production of inflammatory cells and their mediators, and fibroblast activation. Conventional therapy consisting of glucocorticoids or cytotoxic drugs is usually ineffective in preventing progression of the disease. Apoptosis plays a major role in homeostasis as well as proliferation and differentiation. Failure to clear unwanted cells by apoptosis will prolong the inflammation because of the release of their toxic contents. In contrast, excessive apoptosis may cause diseases. DNA damage and apoptosis in lung epithelial and endothelial cells have been reported in acute lung injury and diffuse alveolar damage, as well as pulmonary fibrosis. Protecting epithelial and endothelial cells from injury may be effective and physiological treatment.