Inflammation orchestrates each stage of the life cycle of atherosclerotic plaques. Indeed, inflammatory mediators likely link many traditional and emerging risk factors with atherogenesis. Atheroma initiation involves endothelial activation with recruitment of leucocytes to the arterial intima, where they interact with lipoproteins or their derivatives that have accumulated in this layer. The prolonged and usually clinically silent progression of atherosclerosis involves periods of smouldering inflammation, punctuated by episodes of acute activation that may arise from inflammatory mediators released from sites of extravascular injury or infection or from subclinical disruptions of the plaque. Smooth muscle cells and infiltrating leucocytes can proliferate but also undergo various forms of cell death that typically lead to formation of a lipid-rich ‘necrotic’ core within the evolving intimal lesion. Extracellular matrix synthesized by smooth muscle cells can form a fibrous cap that overlies the lesion’s core. Thus, during progression of atheroma, cells not only procreate but perish. Inflammatory mediators participate in both processes. The ultimate clinical complication of atherosclerotic plaques involves disruption that provokes thrombosis, either by fracture of the plaque’s fibrous cap or superficial erosion. The consequent clots can cause acute ischaemic syndromes if they embarrass perfusion. Incorporation of the thrombi can promote plaque healing and progressive intimal thickening that can aggravate stenosis and further limit downstream blood flow. Inflammatory mediators regulate many aspects of both plaque disruption and healing process. Thus, inflammatory processes contribute to all phases of the life cycle of atherosclerotic plaques, and represent ripe targets for mitigating the disease.

中文翻译：

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动脉粥样硬化斑块生命周期中的炎症


炎症协调动脉粥样硬化斑块生命周期的每个阶段。事实上，炎症介质可能将许多传统和新兴危险因素与动脉粥样硬化联系起来。动脉粥样硬化的发生涉及内皮细胞活化，白细胞募集到动脉内膜，在那里它们与该层中积累的脂蛋白或其衍生物相互作用。动脉粥样硬化的长期且通常在临床上无症状的进展涉及闷烧炎症的时期，其间断的是急性激活的发作，所述急性激活可能是由血管外损伤或感染部位释放的炎症介质或斑块的亚临床破坏引起的。平滑肌细胞和浸润白细胞可以增殖，但也会经历各种形式的细胞死亡，通常导致不断发展的内膜病变内形成富含脂质的“坏死”核心。由平滑肌细胞合成的细胞外基质可以形成覆盖病变核心的纤维帽。因此，在动脉粥样硬化的进展过程中，细胞不仅繁殖而且死亡。炎症介质参与这两个过程。动脉粥样硬化斑块的最终临床并发症涉及通过斑块纤维帽破裂或表面侵蚀引起血栓形成的破坏。如果随之而来的血栓阻碍灌注，可能会导致急性缺血综合征。血栓的合并可以促进斑块愈合和进行性内膜增厚，从而加剧狭窄并进一步限制下游血流。炎症介质调节斑块破坏和愈合过程的许多方面。 因此，炎症过程对动脉粥样硬化斑块生命周期的所有阶段都有贡献，并且代表了缓解该疾病的成熟目标。