Fibrogenesis V.: TGF-β signaling pathways

被引：137

作者：

Wells, RG

机构：

[1] Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06520 USA

[2] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06520 USA

来源：

AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY | 2000年 / 279卷 / 05期

关键词：

fibrosis; extracellular matrix; transforming growth factor-beta receptors; Smads;

D O I：

10.1152/ajpgi.2000.279.5.G845

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

Transforming growth factor (TGF)-beta is a multifunctional peptide growth factor with a wide range of potential effects on growth, differentiation, extracellular matrix deposition, and the immune response. General TGF-beta signaling pathways have been described in detail over the last several years, but factors that determine the nature of the TGF-beta response are poorly understood. In particular, signaling pathways that specifically mediate the matrix effects of TGF-beta have received little attention, although they will be important therapeutic targets in the treatment of pathological fibrosis. This themes article focuses on TGF-beta signaling and highlights potential points for generating matrix-specific responses.

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收藏

页码：G845 / G850

页数：6

相关论文

共 37 条

[1] Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response [J].

Ashcroft, GS ;

Yang, X ;

Glick, AB ;

Weinstein, M ;

Letterio, JJ ;

Mizel, DE ;

Anzano, M ;

Greenwell-Wild, T ;

Wahl, SM ;

Deng, CX ;

Roberts, AB .

NATURE CELL BIOLOGY, 1999, 1 (05) :260-266

[2] TGF-β and fibrosis [J].

Branton, MH ;

Kopp, JB .

MICROBES AND INFECTION, 1999, 1 (15) :1349-1365

[3] INACTIVATION OF THE TYPE-II RECEPTOR REVEALS 2 RECEPTOR PATHWAYS FOR THE DIVERSE TGF-BETA ACTIVITIES [J].

CHEN, RH ;

EBNER, R ;

DERYNCK, R .

SCIENCE, 1993, 260 (5112) :1335-1338

[4] Smad2 transduces common signals from receptor serine-threonine and tyrosine kinases [J].

de Caestecker, MP ;

Parks, WT ;

Frank, CJ ;

Castagnino, P ;

Bottaro, DP ;

Roberts, AB ;

Lechleider, RJ .

GENES & DEVELOPMENT, 1998, 12 (11) :1587-1592

[5] Modulation of transforming growth factor β response and signaling during transdifferentiation of rat hepatic stellate cells to myofibroblasts [J].

Dooley, S ;

Delvoux, B ;

Lahme, B ;

Mangasser-Stephan, K ;

Gressner, AM .

HEPATOLOGY, 2000, 31 (05) :1094-1106

[6] In vivo inhibition of rat stellate cell activation by soluble transforming growth factor β type II receptor:: A potential new therapy for hepatic fibrosis [J].

George, J ;

Roulot, D ;

Koteliansky, VE ;

Bissell, DM .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (22) :12719-12724

[7]

HEINO J, 1989, J BIOL CHEM, V264, P380

[8] TGF-β induces fibronectin synthesis through a c-Jun N-terminal kinase-dependent, Smad4-independent pathway [J].

Hocevar, BA ;

Brown, TL ;

Howe, PH .

EMBO JOURNAL, 1999, 18 (05) :1345-1356

[9] Synergistic cooperation of TFE3 and Smad proteins in TGF-β-induced transcription of the plasminogen activator inhibitor-1 gene [J].

Hua, XX ;

Liu, XD ;

Ansari, DO ;

Lodish, HF .

GENES & DEVELOPMENT, 1998, 12 (19) :3084-3095

[10] EXPRESSION OF VARIANT FIBRONECTINS IN WOUND-HEALING - CELLULAR SOURCE AND BIOLOGICAL-ACTIVITY OF THE EIIIA SEGMENT IN RAT HEPATIC FIBROGENESIS [J].

JARNAGIN, WR ;

ROCKEY, DC ;

KOTELIANSKY, VE ;

WANG, SS ;

BISSELL, DM .

JOURNAL OF CELL BIOLOGY, 1994, 127 (06) :2037-2048

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