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Integrin-Mediated Transforming Growth Factor-β Activation, a Potential Therapeutic Target in Fibrogenic Disorders

被引：140
作者：
Nishimura, Stephen L. [1 ]
机构：
[1] Univ Calif San Francisco, Dept Anat Pathol, San Francisco, CA 94143 USA
来源：
AMERICAN JOURNAL OF PATHOLOGY | 2009年 / 175卷 / 04期
基金：
美国国家卫生研究院;
关键词：
LATENT TGF-BETA; ACUTE LUNG INJURY; SUPERFAMILY SIGNALING PATHWAYS; RELAPSING MULTIPLE-SCLEROSIS; EXTRACELLULAR-MATRIX; PULMONARY-FIBROSIS; IN-VIVO; ALPHA-V-BETA-8-MEDIATED ACTIVATION; VASCULAR MORPHOGENESIS; MESENCHYMAL TRANSITION;
D O I：
10.2353/ajpath.2009.090393
中图分类号：
R36 [病理学];
学科分类号：
100103 [病原生物学];
摘要：
A subset of integrins function as cell surface receptors for the profibrotic cytokine transforming growth factor-beta (TGF-beta). TGF-beta is expressed in an inactive or latent form, and activation of TGF-beta is a major mechanism that regulates TGF-beta function. indeed, important TGF-beta activation mechanisms involve several of the TGF-beta binding integrins. Knockout mice suggest essential roles for integrin-mediated TGF-beta activation in vessel and craniofacial morphogenesis during development and in immune homeostasis and the fibrotic wound heating response in the adult. Amplification of integrin-mediated TGF-beta activation in fibrotic disorders and data from preclinical models suggest that integrins may therefore represent novel targets for antifibrotic therapies. (Am J Pathol 2009, 175:1362-1370; DOI. 10.2353/ajpath.2009.090393)
引用
收藏
页码：1362 / 1370
页数：9
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