Inflammation in atherosclerosis.
Inflammation in atherosclerosis.
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动脉粥样硬化的炎症。
DOI：
10.1161/atvbaha.108.179705
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发表时间：
2012-09
期刊：
影响因子：
--
通讯作者：
Libby P
中科院分区：
文献类型：
--
作者：
Libby P
实验工作阐明了促进动脉粥样硬化的炎症的分子和细胞途径。解开细胞因子作为炎症信使的作用提供了一种机制，即动脉粥样硬化的危险因素可以改变动脉生物学，并产生有利于动脉粥样硬化血栓形成事件的全身环境。移植物动脉硬化的免疫基础的发现表明，即使在没有传统危险因素的情况下，炎症本身也可以推动动脉增生。炎症调节斑块生物学的某些方面，从而触发动脉粥样硬化的血栓并发症。将这些发现转化为人类，既使新的机械洞察力成为可能，也使临床取得了实际进展。
Experimental work has elucidated molecular and cellular pathways of inflammation that promote atherosclerosis. Unraveling the roles of cytokines as inflammatory messengers provided a mechanism whereby risk factors for atherosclerosis can alter arterial biology, and produce a systemic milieu that favors atherothrombotic events. The discovery of the immune basis of allograft arteriosclerosis demonstrated that inflammation per se can drive arterial hyperplasia, even in the absence of traditional risk factors. Inflammation regulates aspects of plaque biology that trigger the thrombotic complications of atherosclerosis. Translation of these discoveries to humans has enabled both novel mechanistic insights and practical clinical advances.