TGF-β signaling in vascular biology and dysfunction

被引：464
作者：
Goumans, Marie-Jose [1 ,2 ]
Liu, Zhen [1 ,2 ]
ten Dijke, Peter [1 ,2 ]
机构：
[1] Leiden Univ, Med Ctr, Dept Mol Cell Biol, NL-2300 RC Leiden, Netherlands
[2] Leiden Univ, Med Ctr, Ctr Biomed Genet, NL-2300 RC Leiden, Netherlands
来源：
CELL RESEARCH | 2009年 / 19卷 / 01期
关键词：
angiogenesis; BMP; Marfan syndrome; Smad; pre-eclampsia; pulmonary hypertension; TGF-beta; TRANSFORMING-GROWTH-FACTOR; SMOOTH-MUSCLE-CELLS; HEREDITARY HEMORRHAGIC TELANGIECTASIA; BONE MORPHOGENETIC PROTEIN; PULMONARY ARTERIAL-HYPERTENSION; RECEPTOR-LIKE KINASE-1; ENDOGLIN HETEROZYGOUS MICE; ENDOTHELIAL-CELLS; II RECEPTOR; GENE-EXPRESSION;
D O I：
10.1038/cr.2008.326
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Transforming growth factor (TGF)-beta family members are multifunctional cytokines that elicit their effects on cells, including endothelial and mural cells, via specific type I and type II serine/threonine kinase receptors and intracellular Smad transcription factors. Knock-out mouse models for TGF-beta family signaling pathway components have revealed their critical importance in proper yolk sac angiogenesis. Genetic studies in humans have linked mutations in these signaling components to specific cardiovascular syndromes such as hereditary hemorrhagic telangiectasia, primary pulmonary hypertension and Marfan syndrome. In this review, we present recent advances in our understanding of the role of TGF-beta receptor signaling in vascular biology and disease, and discuss how this may be applied therapy.
引用
收藏
页码：116 / 127
页数：12
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