Department of Medicine, Pulmonary and Critical Care Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
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.
纤维性疾病，如特发性肺纤维化或硬皮病（系统性硬化症），是慢性纤维增生性疾病，目前尚无有效治疗方法。失调的正常组织修复过程被认为会导致纤维反应，最终由于细胞外基质过度沉积而导致器官功能受损。纤维化病理生理学的机制尚不清楚。最近的研究结果表明，粘着斑激酶（FAK）在纤维性疾病的发展中起着关键作用，它似乎是抗纤维化治疗的一个有吸引力的靶点。在这里，我们回顾了 FAK 作为纤维性信号关键调节剂的新作用及其作为对抗纤维化的未来治疗靶点的潜力。
