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.