Inflammation in atherosclerosis: from pathophysiology to practice.
Inflammation in atherosclerosis: from pathophysiology to practice.
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DOI：
10.1016/j.jacc.2009.09.009
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发表时间：
2009-12-01
影响因子：
24
通讯作者：
Hansson, Goran K.
中科院分区：
文献类型：
--
作者：
Libby, Peter;Ridker, Paul M.;Hansson, Goran K.
就在三十年前，流行的观点将动脉粥样硬化视为一种温和的增生过程。根据这一概念，内皮剥脱损伤导致血小板聚集和血小板源性生长因子的释放，这将触发动脉内膜中平滑肌细胞的增殖，并形成动脉粥样硬化斑块的病灶。动脉粥样硬化的细胞模型更新了Virchow在世纪中期提出的动脉粥样硬化是对损伤的反应的概念。动脉粥样硬化的细胞生物学时代的到来取代了动脉粥样硬化作为脂质碎片在动脉壁上的被动沉积的简单概念。除了在动脉粥样硬化病变中长期认识到的血管平滑肌细胞之外，随后的工作确定了在动脉粥样硬化中起作用的免疫细胞和介质，涉及疾病发展中的炎症机制。基因靶向技术的出现使得能够测试特定分子在小鼠实验性动脉粥样硬化发展中的作用。这些数据证明了高胆固醇血症的关键作用，也支持免疫机制参与动脉粥样硬化的发病机制。 多个独立的证据途径现在指出炎症是一个关键的调节过程，将动脉粥样硬化及其并发症的多种危险因素与动脉生物学改变联系起来。这场关于动脉粥样硬化病理生理学的思想革命已经开始提供临床见解和实用工具，可能有助于患者管理。本文综述了炎症在动脉粥样硬化形成中的作用，并强调了基础科学的这些进展如何改变临床实践。
Just three decades ago the prevailing viewpoint envisaged atherosclerosis as a bland proliferative process. According to that concept, endothelial denuding injury led to platelet aggregation and release of platelet-derived growth factor which would trigger the proliferation of smooth muscle cells in the arterial intima, and form the nidus of the atherosclerotic plaque. This cellular model of atherosclerosis updated Virchow's concepts of atherosclerosis as a response to injury formulated in the mid-nineteenth century. The advent of the cell biological era of atherosclerosis supplanted the simplistic concept of the atheroma as a passive deposition of lipid debris on the artery wall. Beyond the vascular smooth muscle cells long recognized in atherosclerotic lesions, subsequent work identified immune cells and mediators at work in atheromata, implicating inflammatory mechanisms in disease development. The advent of gene-targeting technology enabled the testing of the roles of specific molecules in the development of experimental atherosclerosis in mice. Such data demonstrated a critical role for hypercholesterolemia and also supported the participation of immune mechanisms in the pathogenesis of atherosclerosis. Multiple independent pathways of evidence now pinpoint inflammation as a key regulatory process that links multiple risk factors for atherosclerosis and its complications with altered arterial biology. This revolution in our thinking about the pathophysiology of atherosclerosis has begun to provide clinical insight and practical tools that may aid patient management. This review provides an update of the role of inflammation in atherogenesis and highlights how translation of these advances in basic science promises to change clinical practice.
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影响因子：
6.5
作者：
Hartvigsen, Karsten;Chou, Meng-Yun;Witztum, Joseph L.
通讯作者：
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蛋白水解活性动脉粥样硬化中炎症的实时导管分子传感。
影响因子：
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作者：
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通讯作者：
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作者：
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3.2
作者：
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通讯作者：
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影响因子：
15.9
作者：
Binder, CJ;Hartvigsen, K;Witztum, JL
通讯作者：
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