TGF-β signaling in fibrosis

被引：1048

作者：

Biernacka, Anna ^{[1
]}

Dobaczewski, Marcin ^{[1
]}

Frangogiannis, Nikolaos G. ^{[1
]}

机构：

[1] Albert Einstein Coll Med, Div Cardiol, Bronx, NY 10461 USA

来源：

GROWTH FACTORS | 2011年 / 29卷 / 05期

关键词：

TGF-beta; fibrosis; collagen; Smad; MAPK; GROWTH-FACTOR-BETA; MESENCHYMAL TRANSITION; EXTRACELLULAR-MATRIX; CARDIAC FIBROSIS; TRANSFORMING GROWTH-FACTOR-BETA-1; PULMONARY-FIBROSIS; LUNG FIBROSIS; ACTIVATION; FIBROBLASTS; KINASE;

D O I：

10.3109/08977194.2011.595714

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Transforming growth factor beta (TGF-beta) is a central mediator of fibrogenesis. TGF-beta is upregulated and activated in fibrotic diseases and modulates fibroblast phenotype and function, inducing myofibroblast transdifferentiation while promoting matrix preservation. Studies in a wide range of experimental models have demonstrated the involvement of the canonical activin receptor-like kinase 5/Smad3 pathway in fibrosis. Smad-independent pathways may regulate Smad activation and, under certain conditions, may directly transduce fibrogenic signals. The profibrotic actions of TGF-beta are mediated, at least in part, through induction of its downstream effector, connective tissue growth factor. In light of its essential role in the pathogenesis of fibrosis, TGF-beta has emerged as an attractive therapeutic target. However, the pleiotropic and multifunctional effects of TGF-beta and its role in tissue homeostasis, immunity and cell proliferation raise concerns regarding potential side effects that may be caused by TGF-beta blockade. This minireview summarizes the role of TGF-beta signaling pathways in the fibrotic response.

引用

页码：196 / 202

页数：7

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