ABSTRACT
Recent studies support the involvement of disordered pathways of fibrin turnover and extravascular fibrin deposition in the pathogenesis of pulmonary fibrosis. Alveolar fibrin deposition is commonly associated with alveolar injury. The fibrinous neomatrix undergoes progressive remodeling and scarring after acute lung injury and in the interstitial lung diseases. Changes in local fibrin turnover favor increased fibrin formation and delayed fibrin clearance under these circumstances. These changes are predicated on the responses of alveolar macrophages, the lung epithelium, and lung fibroblasts to inflammatory mediators. In all, the events associated with scarring in the lung parenchyma recapitulates the central events that characterize wound healing. Recent interventional strategies designed to reverse basic derangements of local fibrin turnover have been successful in sepsis and pleural injury, raising the possibility that similar approaches could be extrapolated to prevent scarring in the injured lung itself.
