动脉粥样硬化
炎症
炎症反应
医学
巨噬细胞
血栓形成
下调和上调
免疫学
生物信息学
内科学
生物
心脏病学
生物化学
基因
体外
出处
期刊:Nature
[Springer Nature]
日期:2002-12-01
卷期号:420 (6917): 868-874
被引量:7983
摘要
Abundant data link hypercholesterolaemia to atherogenesis. However, only recently have we appreciated that inflammatory mechanisms couple dyslipidaemia to atheroma formation. Leukocyte recruitment and expression of pro-inflammatory cytokines characterize early atherogenesis, and malfunction of inflammatory mediators mutes atheroma formation in mice. Moreover, inflammatory pathways promote thrombosis, a late and dreaded complication of atherosclerosis responsible for myocardial infarctions and most strokes. The new appreciation of the role of inflammation in atherosclerosis provides a mechanistic framework for understanding the clinical benefits of lipid-lowering therapies. Identifying the triggers for inflammation and unravelling the details of inflammatory pathways may eventually furnish new therapeutic targets.
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