Pathogenesis of fibrosis:: role of TGF-β and CTGF

被引：278

作者：

Ihn, H ^{[1
]}

机构：

[1] Univ Tokyo, Fac Med, Dept Dermatol, Bunkyo Ku, Tokyo 1138655, Japan

来源：

CURRENT OPINION IN RHEUMATOLOGY | 2002年 / 14卷 / 06期

关键词：

D O I：

10.1097/00002281-200211000-00009

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Transforming growth factor (TGF)-beta regulates diverse biologic activities including cell growth, cell death or apoptosis, cell differentiation, and extracellular matrix (ECM) synthesis. TGF-beta is believed to be a key mediator of tissue fibrosis as a consequence of ECM accumulation in pathologic states such as systemic sclerosis. TGF-beta is known to induce the expression of ECM proteins in mesenchymal cells, and to stimulate the production of protease inhibitors that prevent enzymatic breakdown of the ECM. Connective tissue growth factor (CTGF), which is induced by TGF-beta, has been reported to mediate stimulatory actions of TGF-beta ECM synthesis. This review focuses on the possible role of TGF-beta and CTGF in the pathogenesis of fibrosis.

引用

页码：681 / 685

页数：5

共 78 条

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