TGF-beta and fibrosis

Citation
Mh. Branton et Jb. Kopp, TGF-beta and fibrosis, MICROBES IN, 1(15), 1999, pp. 1349-1365
Citations number
228
Categorie Soggetti
Immunology
Journal title
MICROBES AND INFECTION
ISSN journal
12864579 → ACNP
Volume
1
Issue
15
Year of publication
1999
Pages
1349 - 1365
Database
ISI
SICI code
1286-4579(199912)1:15<1349:TAF>2.0.ZU;2-C
Abstract
Transforming growth factor-beta (TGF-beta) isoforms are multifunctional cyt okines that play a central role in wound healing and in tissue repair. TGF- beta is found in all tissues, bm is particularly abundant in bone, lung, ki dney and placental tissue. TGF-beta is produced by many but not all parench ymal cell types, and is also produced or released by infiltrating cells suc h as lymphocytes, monocytes/macrophages, and platelets. Following wounding or inflammation, all these cells are potential sources of TGF-beta. In gene ral, the release and activation of TGF-beta stimulates the production of va rious extracellular matrix proteins and inhibits the degradation of these m atrix proteins, although exceptions to these principles abound. These actio ns of TGF-beta contribute to tissue repair, which under ideal circumstances leads to the restoration of normal tissue architecture and may involve a c omponent of tissue fibrosis. In many diseases, excessive TGF-beta contribut es to a pathologic excess of tissue fibrosis that compromises normal organ function, a topic that has been the subject of numerous reviews [1-3]. In t he following chapter, we will discuss the role of TGF-beta in tissue fibros is, with particular emphasis on renal fibrosis. (C) 1999 Editions scientifi ques et medicales Elsevier SAS.