Targeting focal adhesion kinase in fibrotic diseases

BioDrugs. 2013 Feb;27(1):15-23. doi: 10.1007/s40259-012-0003-4.


Fibrotic diseases such as idiopathic pulmonary fibrosis or scleroderma (systemic sclerosis) are chronic fibroproliferative disorders for which there are currently no effective treatments. Dysregulated normal tissue repair process is considered to cause a fibrotic response culminating in compromised organ function due to excess extracellular matrix deposition. The mechanisms underlying the pathophysiology of fibrosis are poorly understood. Recent findings suggest that focal adhesion kinase (FAK) plays a key role in development of fibrotic disorders, and it appears to be an attractive target for antifibrotic therapy. Here, we review the emerging role of FAK as a key regulator of fibrotic signaling and its potential as a future therapeutic target to counteract fibrosis.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Differentiation / drug effects
  • Cell Differentiation / physiology
  • Cell Movement / drug effects
  • Cell Movement / physiology
  • Cell Survival / drug effects
  • Focal Adhesion Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Humans
  • Myofibroblasts / drug effects
  • Myofibroblasts / enzymology
  • Myofibroblasts / pathology
  • Protein Kinase Inhibitors / administration & dosage
  • Protein Kinase Inhibitors / therapeutic use*
  • Pulmonary Fibrosis / drug therapy*
  • Pulmonary Fibrosis / enzymology
  • Pulmonary Fibrosis / pathology
  • Scleroderma, Systemic / drug therapy*
  • Scleroderma, Systemic / enzymology
  • Scleroderma, Systemic / pathology


  • Protein Kinase Inhibitors
  • Focal Adhesion Protein-Tyrosine Kinases