作者: David Lagares , Mohit Kapoor
DOI: 10.1007/S40259-012-0003-4
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摘要: Fibrotic diseases such as idiopathic pulmonary fibrosis or scleroderma (systemic sclerosis) are chronic fibroproliferative disorders for which there currently no effective treatments. Dysregulated normal tissue repair process is considered to cause a fibrotic response culminating in compromised organ function due excess extracellular matrix deposition. The mechanisms underlying the pathophysiology of poorly understood. Recent findings suggest that focal adhesion kinase (FAK) plays key role development disorders, and it appears be an attractive target antifibrotic therapy. Here, we review emerging FAK regulator signaling its potential future therapeutic counteract fibrosis.