动脉,炎症和胰岛素抵抗。

Jacques Amar, Laurence Perez, Rémi Burcelin, Bernard Chamontin
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引用次数: 12

摘要

从斑块形成到破裂,炎症在动脉粥样硬化的各个阶段都起作用。在炎症介质的引导下,单核细胞与被心血管危险因素损伤的内皮结合,然后向内膜迁移,在内膜中加入氧化的低密度脂蛋白颗粒后,它们转化为泡沫细胞。脂质条纹形成并发展为动脉粥样硬化斑块,易发生侵蚀和破裂。过量脂肪组织引起的炎症降低了胰岛素敏感性,这是代谢综合征的主要特征。因此,炎症似乎是动脉粥样硬化和代谢综合征的共同因素。引发这种炎症的因素尚未确定。一种观点似乎指向饮食。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Arteries, inflammation and insulin resistance.

Inflammation plays a role in all stages of atherosclerosis from the formation to the rupture of the plaque. Guided by inflammatory mediators, monocytes bind to an endothelium damaged by cardiovascular risk factors, and then migrate towards the intima where, after incorporating oxidized low-density lipoprotein particles, they are transformed into foam cells. The lipid streak forms and develops as an atherosclerotic plaque, which is susceptible to erosion and rupture. Inflammation fed by excess adipose tissue decreases insulin sensitivity, which is the central feature of the metabolic syndrome. Inflammation therefore appears to be a common factor of atherosclerosis and the metabolic syndrome. The factors triggering this inflammation have yet to be determined. One line of thought would appear to point to diet.

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