title: Focal Adhesion Kinase: A Key Mediator of Transforming Growth Factor Beta Signaling in Fibroblasts.
abstract: CONCLUSIONS
  There is no effective drug therapy for scarring and fibrotic disease. The cytokine transforming growth factor beta (TGF-β) promotes tissue repair, but its excessive action can lead to over exuberant scarring and fibrotic disease. However, owing to the multifunctional nature of TGF-β, broad targeting of the canonical Smad-TGF-β signaling pathwayin vivois likely to have unintended, deleterious consequences.
  
  
  BACKGROUND
  (1) The myofibroblast is the essential cell type that mediates tissue repair and fibrosis. (2) TGF-β is an essential contributor to myofibroblast differentiation and activity. (3) TGF-β selectively promotes tissue repair and fibrosis via the noncanonical focal adhesion kinase (FAK) pathway; FAK mediates myofibroblast differentiation, and hence may represent a novel intervention point for drugs treating fibrotic disease.
  
  
  RESULTS
  Excessive scarring (e.g.,in hypertrophic scars, keloids, and scleroderma) is characterized by enhanced TGF-β signaling and is a major clinical problem. Drugs that selectively and effectively control the profibrotic action of TGF-β is therefore of clinical relevance.
  
  
  CONCLUSIONS
  FAK inhibition may represent a novel therapy for scarring disorders.
authors: Departments of Dentistry and Physiology and Pharmacology, University of Western Ontario , London, Canada .
authors: Andrew
authors: A
authors: Leask