abstract
- A new hypothesis of the pathogenesis of fibroproliferative lung disease suggests that fibrosis is caused by abnormal and excessive wound healing and pathologic tissue remodelling. Inflammation is possibly an epiphenomenon. Cytokines are critical players in the pathologic process and attractive targets for pharmacological intervention. TGF beta is a key profibrotic growth factor, a variety of approaches are known to modify and inhibit its activity. This article reviews the basic pathological concepts of pulmonary fibrogenesis and outlines its potential clinical benefit.