HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Flanders, K. C. Articles by Burmester, J. K. Search for Related Content PubMed PubMed Citation Articles by Flanders, K. C. Articles by Burmester, J. K.

Medical Applications of Transforming Growth Factor-ß

Laboratory of Cell Regulation and Carcinogenesis, National Institutes of Health, Bethesda, Maryland

James K. Burmester, PhD

Personalized Medicine Research Center, Marshfield Medical Research Foundation, Marshfield, Wisconsin

REPRINT REQUESTS: James K. Burmester, PhD, Personalized Medicine Research Center, Marshfield Medical Research Foundation, 1000 North Oak Avenue, Marshfield, WI 54449, Telephone: 715-389-4368, Fax: 715-389-3808, Email: burmester.james{at}marshfieldclinic.org

Abstract

Transforming growth factor-ß (TGF-ß) proteins and their antagonists have entered clinical trials. These multi-functional regulators of cell growth and differentiation induce extracellular matrix proteins and suppress the immune system making TGF-ßs useful in treatment of wounds with impaired healing, mucositis, fractures, ischemia-reperfusion injuries, and autoimmune disease. In diseases such as keloids, glomerulonephritis and pulmonary fibrosis, excessive expression of TGF-ß has been implicated as being responsible for accumulation of detrimental scar tissue. In these conditions, agents that block TGF-ß have prevented or reversed disease. Similarly, in carcinogenesis, blocking TGF-ß activity may be valuable in stimulating an immune response towards metastasis. As these blocking agents receive approval, we will likely have new therapies for previously recalcitrant diseases.

Key Words: Fibrosis • Cancer • Immunosuppression • Knockout mice

This article has been cited by other articles:

				B R Klass, A O Grobbelaar, and K J Rolfe Transforming growth factor {beta}1 signalling, wound healing and repair: a multifunctional cytokine with clinical implications for wound repair, a delicate balance Postgrad. Med. J., January 1, 2009; 85(999): 9 - 14. [Abstract] [Full Text] [PDF]

				C. D. Keller, P. Rivera Gil, M. Tolle, M. van der Giet, J. Chun, H. H. Radeke, M. Schafer-Korting, and B. Kleuser Immunomodulator FTY720 Induces Myofibroblast Differentiation via the Lysophospholipid Receptor S1P3 and Smad3 Signaling Am. J. Pathol., January 1, 2007; 170(1): 281 - 292. [Abstract] [Full Text] [PDF]