ATF-4 and vascular injury: integration of growth factor signaling and the cellular stress response.
ATF-4 and vascular injury: integration of growth factor signaling and the cellular stress response.
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ATF-4 和血管损伤：生长因子信号传导和细胞应激反应的整合。
DOI：
10.1161/circresaha.108.182246
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发表时间：
2008
影响因子：
20.1
通讯作者：
Chin,MichaelT
中科院分区：
文献类型：
--
作者：
Chin,MichaelT
Smooth muscle proliferation and neointimal formation are characteristic features of vascular lesions that develop after vascular injury and contribute to the development of occlusive vascular lesions after percutaneous coronary interventions and in transplant vasculopathy. The traditional model for the development of these vascular lesions has postulated that a complex interplay among locally released growth factors and cytokines, circulating platelets and inflammatory cells, local smooth muscle and endothelial cells, and perhaps circulating precursor cells involving multiple cellular processes such as adhesion, proliferation, migration, and apoptosis is orchestrated at many levels, resulting in vascular stenosis. The temporal and spatial complexity of the overall process and the diverse contributions of various components have provided many opportunities for study, but identifying and linking the various critical steps in the development of occlusive vascular lesions has remained challenging. Although numerous studies examining roles of vascular signaling pathways and vascular transcription factors have been published, a clear picture of how signaling and transcription are intertwined remains elusive. In this issue of Circulation Research, Malabanan et al present a comprehensive series of experiments linking the transcription factor activating transcription factor (ATF)-4 to intimal thickening after injury and identify both upstream and downstream associated growth factor pathways, thereby providing additional insight into the orchestrated activation of transcriptional and signaling pathways in vascular disease. 1The authors initially identified ATF-4 as a potential regulator of neointimal formation through a microarray screen for genes induced in smooth muscle cells (SMCs) by fibroblast growth factor (FGF)-2. FGF-2 has been identified previously as a major smooth muscle mitogen and has been implicated in the pathogenesis of atherosclerosis and restenosis after angioplasty. 2–4 FGF-2 is normally stored and rapidly secreted after injury3 and functions in both an autocrine and paracrine fashion. To confirm the microarray findings and determine their relevance in vivo, the authors examined the expression of ATF-4 in both a rat model of carotid artery balloon injury and in an in vitro model of SMC injury. As expected, they
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DOI：
10.1046/j.1365-2362.2003.01223.x
发表时间：
2003-10-01
影响因子：
5.5
作者：
Belgore, F;Lip, GYH;Blann, AD
通讯作者：
Blann, AD
影响因子：
15.9
作者：
BROGI, E;WINKLES, JA;LIBBY, P
通讯作者：
LIBBY, P
血管内皮生长因子通过表达 fms 样酪氨酸激酶 1 来增加体内血管平滑肌细胞对成纤维细胞生长因子 2 的有丝分裂反应。
影响因子：
20.1
作者：
Leslie L. Couper;Shane R. Bryant;J. Eldrup;Carl E. Bredenberg;V. Lindner
通讯作者：
V. Lindner
猪动脉修复过程中血管内皮生长因子（VEGF）的表达。
DOI：
10.1016/s1078-5884(98)80180-9
发表时间：
1998
期刊：
European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery
影响因子：
--
作者：
S. Wysocki;Ming Zheng;Anne Smith;Paul Norman
通讯作者：
Paul Norman
影响因子：
37.8
作者：
ASAHARA, T;BAUTERS, C;ISNER, JM
通讯作者：
ISNER, JM