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

[61] Blockade of type β transforming growth factor signaling prevents liver fibrosis and dysfunction in the rat
Qi, Z
Atsuchi, N
Ooshima, A
Takeshita, A
Ueno, H
[J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (05) : 2345 - 2349
[62] Role of transforming growth factor β type II receptor in hepatic fibrosis:: Studies of human chronic hepatitis C and experimental fibrosis in rats
Roulot, D
Sevcsik, AM
Coste, T
Strosberg, AD
Marullo, S
[J]. HEPATOLOGY, 1999, 29 (06) : 1730 - 1738
[63] PLATELET FACTORS STIMULATE FIBROBLASTS AND SMOOTH-MUSCLE CELLS QUIESCENT IN PLASMA SERUM TO PROLIFERATE
RUTHERFORD, RB
ROSS, R
[J]. JOURNAL OF CELL BIOLOGY, 1976, 69 (01) : 196 - 203
[64] Identification of important regions in the cytoplasmic juxtamembrane domain of type I receptor that separate signaling pathways of transforming growth factor-beta
Saitoh, M
Nishitoh, H
Amagasa, T
Miyazono, K
Takagi, M
Ichijo, H
[J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (05) : 2769 - 2775
[65] Role of p38 MAPK in transforming growth factor β stimulation of collagen production by scleroderma and healthy dermal fibroblasts
Sato, M
Shegogue, D
Gore, EA
Smith, EA
Mcdermott, PJ
Trojanowska, M
[J]. JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2002, 118 (04) : 704 - 711
[66] The role of Smad3 in mediating mouse hepatic stellate cell activation
Schnabl, B
Kweon, YO
Frederick, JP
Wang, XF
Rippe, RA
Brenner, DA
[J]. HEPATOLOGY, 2001, 34 (01) : 89 - 100
[67] PROTEIN KINASES .7. THE MAPK SIGNALING CASCADE
SEGER, R
KREBS, EG
[J]. FASEB JOURNAL, 1995, 9 (09) : 726 - 735
[68] A structural basis for mutational inactivation of the tumour suppressor Smad4
Shi, YG
Hata, A
Lo, RS
Massague, J
Pavletich, NP
[J]. NATURE, 1997, 388 (6637) : 87 - 93
[69] Induction of subcutaneous tissue fibrosis in newborn mice by transforming growth factor beta - Simultaneous application with basic fibroblast growth factor causes persistent fibrosis
Shinozaki, M
Kawara, S
Hayashi, N
Kakinuma, T
[J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1997, 237 (02) : 292 - 296
[70] Iloprost suppresses connective tissue growth factor production in fibroblasts and in the skin of scleroderma patients
Stratton, R
Xu, SW
Martini, G
Holmes, A
Leask, A
Haberberger, T
Martin, GR
Black, CM
Abraham, D
[J]. JOURNAL OF CLINICAL INVESTIGATION, 2001, 108 (02) : 241 - 250

← 1 2 3 4 5 6 7 8 →