Macrophages in the pathogenesis of atherosclerosis.

Macrophages in the pathogenesis of atherosclerosis.
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DOI:
10.1016/j.cell.2011.04.005
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发表时间:
2011-04-29
期刊:
影响因子:
64.5
通讯作者:
Tabas I
Tabas I
中科院分区:
生物学1区
文献类型:
--
作者:
Moore KJ;Tabas I

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巨噬细胞正越来越多地被认为是慢性衰老疾病的关键因子,包括癌症、代谢性疾病和动脉粥样硬化。在动脉粥样硬化中,单核细胞对基质保留的载脂蛋白B-脂蛋白作出反应,趋化到动脉内皮下的局灶性区域。单核细胞衍生的巨噬细胞然后参与适应不良的非消退性炎症反应,导致内皮下扩张,伴有额外的细胞、脂质和基质。少数病变发生坏死破坏,引发急性血栓性血管疾病,包括心肌梗死、中风和心源性猝死。这篇综述讨论了巨噬细胞如何促进早期和晚期动脉粥样硬化,重点是由坚实的机制和体内数据支持的概念。
Macrophages are becoming increasingly recognized as key agents in chronic diseases of aging, including cancer, metabolic disease, and, the topic of this review, atherosclerosis. In atherosclerosis, monocytes hone to focal area of the arterial subendothelium in response to matrix-retained apolipoprotein B-lipoproteins. Monocyte-derived macrophages then participate in a maladaptive, non-resolving inflammatory response that leads to subendothelial expansion with additional cells, lipid, and matrix. A few lesions undergo necrotic disruption, triggering acute thrombotic vascular disease, including myocardial infarction, stroke, and sudden cardiac death. This review discusses how macrophages contribute to both early and advanced atherosclerosis, with an emphasis on concepts supported by solid mechanistic and in-vivo data.
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