Integrin-TGF-β crosstalk in fibrosis, cancer and wound healing

被引：494

作者：

Margadant, Coert ^{[1
]}

Sonnenberg, Arnoud ^{[1
]}

机构：

[1] Netherlands Canc Inst, Div Cell Biol, NL-1066 CX Amsterdam, Netherlands

来源：

EMBO REPORTS | 2010年 / 11卷 / 02期

关键词：

integrin; TGF-beta; fibrosis; cancer; wound healing; GROWTH-FACTOR-BETA; EPITHELIAL-MESENCHYMAL TRANSITION; ACTIVATES LATENT TGF-BETA-1; RECEPTOR KINASE INHIBITOR; HUMAN LUNG FIBROBLASTS; ALPHA-V-BETA-6; INTEGRIN; INCREASED EXPRESSION; PULMONARY-FIBROSIS; IN-VIVO; TRANSFORMING GROWTH-FACTOR-BETA-1;

D O I：

10.1038/embor.2009.276

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Accumulating evidence indicates that there is extensive crosstalk between integrins and TGF-beta signalling. TGF-beta affects integrin-mediated cell adhesion and migration by regulating the expression of integrins, their ligands and integrin-associated proteins. Conversely, several integrins directly control TGF-beta activation. In addition, a number of integrins can interfere with both Smad-dependent and Smad-independent TGF-beta signalling in different ways, including the regulation of the expression of TGF-beta signalling pathway components, the physical association of integrins with TGF-beta receptors and the modulation of downstream effectors. Reciprocal TGF-beta-integrin signalling is implicated in normal physiology, as well as in a variety of pathological processes including systemic sclerosis, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease and cancer; thus, integrins could provide attractive therapeutic targets to interfere with TGF-beta signalling in these processes.

引用

页码：97 / 105

页数：9

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