Libby Peter
Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Nature. 2002;420(6917):868-74. doi: 10.1038/nature01323.
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.
大量数据表明高胆固醇血症与动脉粥样硬化的发生有关。然而，直到最近我们才认识到炎症机制将血脂异常与动脉粥样硬化的形成联系起来。白细胞募集和促炎细胞因子的表达是早期动脉粥样硬化形成的特征，炎症介质功能异常会抑制小鼠动脉粥样硬化的形成。此外，炎症途径会促进血栓形成，这是动脉粥样硬化晚期可怕的并发症，可导致心肌梗死和大多数中风。对炎症在动脉粥样硬化中作用的新认识为理解降脂治疗的临床益处提供了一个机制框架。确定炎症的触发因素并阐明炎症途径的细节最终可能会提供新的治疗靶点。
