Transcription factor and kinase-mediated signaling in atherosclerosis and vascular injury

被引：72

作者：

Adhikari N. ^{[1
]}

Charles N. ^{[1
]}

Lehmann U. ^{[1
]}

Hall J.L. ^{[1
]}

机构：

[1] University of Minnesota, Cardiovascular Division, Minneapolis, MN 55455

来源：

Current Atherosclerosis Reports | 2006年 / 8卷 / 3期

关键词：

Vascular Smooth Muscle Cell; Vascular Remodel; Arterioscler Thromb Vasc Biol; Neointimal Formation; Vascular Smooth Muscle Cell Proliferation;

D O I：

10.1007/s11883-006-0081-1

中图分类号：

学科分类号：

摘要：

Our understanding of the molecular signaling pathways regulating the initiation and progression of atherosclerosis or remodeling in response to injury has begun to cross the boundaries from regulation of well-described canonical pathways to the interplay between these pathways. The focus of this review is to summarize our current understanding of a finite group of transcription factors and kinases involved in vascular injury and atherosclerosis, including nuclear factor-κB (NF-κB), early growth response factor-1 (Egr-1), activator protein-1 (AP-1), hypoxia inducible factor-1α (HIF-1α), homeobox, and T cell factor/lymphoid enhancer factor (Tcf-Lef), as well as the kinases janus kinase/signal transducers and activators of transcription (JAK/ STAT), protein kinase C (PKC), p38, Rho, ERK5, JNK, p44/p42, and phosphoinositide 3 (PI3) kinase/AKT. Copyright © 2006 by Current Science Inc.

引用

页码：252 / 260

页数：8

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