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Originally published online as doi:10.2353/ajpath.2009.090393 on September 3, 2009

Published online before print September 3, 2009
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(American Journal of Pathology. 2009;175:1362-1370.)
© 2009 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2009.090393

Review

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

Stephen L. Nishimura

From the Department of Anatomic Pathology, University of California San Francisco, San Francisco, California

A subset of integrins function as cell surface receptors for the profibrotic cytokine transforming growth factor-β (TGF-β). TGF-β is expressed in an inactive or latent form, and activation of TGF-β is a major mechanism that regulates TGF-β function. Indeed, important TGF-β activation mechanisms involve several of the TGF-β binding integrins. Knockout mice suggest essential roles for integrin-mediated TGF-β activation in vessel and craniofacial morphogenesis during development and in immune homeostasis and the fibrotic wound healing response in the adult. Amplification of integrin-mediated TGF-β activation in fibrotic disorders and data from preclinical models suggest that integrins may therefore represent novel targets for antifibrotic therapies.




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J. A. Markovics, J. Araya, S. Cambier, D. Jablons, A. Hill, P. J. Wolters, and S. L. Nishimura
Transcription of the Transforming Growth Factor {beta} Activating Integrin {beta}8 Subunit Is Regulated by SP3, AP-1, and the p38 Pathway
J. Biol. Chem., August 6, 2010; 285(32): 24695 - 24706.
[Abstract] [Full Text] [PDF]


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