title: Targeting focal adhesion kinase in fibrotic diseases.
abstract: 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.
authors: Department of Medicine, Pulmonary and Critical Care Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
authors: David
authors: D
authors: Lagares
authors: Mohit
authors: M
authors: Kapoor
mesh_terms: D000818:Animals; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology; D002465:Cell Movement / Q000187:drug effects / Q000502:physiology; D002470:Cell Survival / Q000187:drug effects; D051416:Focal Adhesion Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors*; D006801:Humans; D058628:Myofibroblasts / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D047428:Protein Kinase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D011658:Pulmonary Fibrosis / Q000188:drug therapy* / Q000201:enzymology / Q000473:pathology; D012595:Scleroderma, Systemic / Q000188:drug therapy* / Q000201:enzymology / Q000473:pathology
chemical_list: D047428:Protein Kinase Inhibitors; D051416:Focal Adhesion Protein-Tyrosine Kinases