Purpose of review Pleural fibrosis is a double-edged sword in clinical settings. Successful induction of pleural fibrosis is the basis of therapeutic pleurodesis. On the other hand, pleural septations and fibrosis are undesirable outcomes in pleural infection and fibrothoraces. The significance of growth factors in the pathogenesis of pleural fibrosis has become increasingly apparent.Recent findings Recent findings have indicated that transforming growth factor beta is a key mediator of pleural fibrosis and demonstrated the therapeutic potential of both transforming growth factor beta itself and transforming growth factor beta inhibitor. Basic fibroblast growth factor has been highlighted as a key factor in successful pleurodesis, and in the formation of pleural effusions. Vascular endothelial growth factor inhibition has been shown to decrease pleural fibrosis in vivo. By contrast, hepatocyte growth factor stimulates non-fibrotic healing, while inhibition increases fibrosis.Summary The actions of the growth factors, and their inhibitors, are potentially and/or currently applicable in a clinical setting. Understanding the biology of these growth factors may allow therapeutic manipulation of these cytokines to create pleurodesis or to inhibit pleural (and peritoneal) adhesion/fibrosis.
|Journal||Current Opinion in Pulmonary Medicine|
|Publication status||Published - 2006|