Endothelin-1-induced signaling pathways in vascular smooth muscle cells

被引:121
作者
Bouallegue, Ali [1 ]
Daou, Grace Bou [1 ]
Srivastava, Ashok K. [1 ]
机构
[1] Univ Montreal, Dept Med, Montreal, PQ H1W 4A4, Canada
关键词
endothelin-1; vascular smooth muscle cells; MAPKs; PKB/Akt; PI3-K; PKC; vascular diseases;
D O I
10.2174/157016107779317161
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Endothelin-1 (ET-1), a vasoactive peptide, is believed to contribute to the pathogenesis of vascular abnormalities such as hypertension, atherosclerosis, hypertrophy and restenosis. ET-1 elicits its biological effects through the activation of two receptor subtypes, ET-A and ET-B that belong to a large family of transmembrane guanine nucleotide-binding protein-coupled receptors (GPCRs). ET-1 receptor activation results in the stimulation of several signaling pathways including mitogen-activated protein kinases (MAPKs), phosphatidylinositol 3-kinase (PI3-K) and protein kinase B (PKB). An intermediary role of Ca2+/calmodulin-dependent protein kinases (CaMK), protein kinase C (PKC) as well as receptor and non-receptor protein tyrosine kinases in triggering the activation of MAPK and PI3-K/PKB signaling in response to ET-1 has been suggested. Activation of these pathways by ET-1 is intimately linked with the regulation of cellular hypertrophy, growth, proliferation and cell survival. Here we provide an overview of these signaling pathways in vascular smooth muscle cells (VSMCs) with an emphasis on their potential role in vascular pathophysiology.
引用
收藏
页码:45 / 52
页数:8
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