Vascular smooth muscle cell proliferation in restenosis.
Vascular smooth muscle cell proliferation in restenosis.
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DOI：
10.1161/circinterventions.110.957332
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发表时间：
2011-02-01
期刊：
影响因子：
--
通讯作者：
Marks AR
中科院分区：
文献类型：
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作者：
Marx SO;Totary-Jain H;Marks AR
目前用于恢复狭窄血管中的血流的治疗方法涉及使用经皮装置和冠状动脉旁路手术。在破坏血管正常完整性的所有手术中，血管腔狭窄（称为再狭窄）的发生率增加。缓解，任意定义为与参考血管相比血管直径狭窄超过50%，受遗传背景和影响心血管系统的疾病（包括糖尿病、高血压和高胆固醇血症）的调节。在20世纪70年代，Andreas Gruntzig率先使用冠状动脉经腔扩张治疗症状性冠状动脉疾病，并报告了19%的再狭窄率（32例患者中的6例）。1-3随后的研究表明再狭窄率约为33%。4 25年后，尽管采用药物和机械方法降低了再狭窄的发生率，但它仍然是一个重大问题，特别是在高风险患者群体中，限制了整体成功。经皮介入治疗后的再灌注表现为血小板聚集、生长因子释放、炎性细胞浸润、中膜平滑肌细胞增殖和迁移以及细胞外基质重塑。血管对损伤的反应不仅取决于血管内的细胞，而且还受到循环的骨髓源性细胞的调节。了解生理性愈合反应和病理性再狭窄反应的分子机制一直是广泛研究的焦点，这导致了控制新生内膜病理形成的新方法的发展。在这篇综述中，我们将重点关注导致异常新生内膜增生的一些分子机制，特别是血管平滑肌中的细胞周期和微小RNA（miRNA）。
Current therapeutic approaches to restore blood flow in stenotic blood vessels involve the use of percutaneous devices and coronary bypass surgery. In all procedures that disrupt the normal integrity of the blood vessels, there is an increased incidence of vessel luminal narrowing, termed restenosis. Restenosis, arbitrarily defined as greater than 50% narrowing of vessel diameter compared with the reference vessel, is modulated by genetic background and diseases that affect the cardiovascular system, including diabetes, hypertension, and hypercholesterolemia. In the 1970s, Andreas Gruntzig pioneered the use of transluminal dilatation of coronary arteries for symptomatic coronary artery disease and reported a 19% rate of restenosis (6 of 32 patients). 1–3 Subsequent studies demonstrated a restenosis rate of approximately 33%. 4 More than 25 years later, despite pharmacological and mechanical approaches to reduce the incidence of restenosis, it remains a significant problem, especially in high-risk patient groups, limiting overall success. Restenosis after percutaneous intervention is characterized by platelet aggregation, release of growth factors, inflammatory cell infiltration, medial smooth muscle cell proliferation and migration, and extracellular matrix remodeling. The vascular response to injury depends not only on the cells within the vessels but is also modulated by circulating bone marrow–derived cells. Understanding the molecular mechanisms underlying the physiological healing response and the pathological restenosis response has been the focus of extensive investigations, which have led to the development of novel approaches to control the pathological formation of the neointima. In this review, we will focus on some of the molecular mechanisms responsible for the abnormal neointimal hyperplasia, specifically focusing on cell cycle and microRNA (miRNA) in the vascular smooth muscle.