Cholesterol crystals and inflammation.

Cholesterol crystals and inflammation.
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DOI:
10.1007/s11926-012-0313-z
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发表时间:
2013-03
影响因子:
5
通讯作者:
Latz, Eicke
Latz, Eicke
中科院分区:
医学2区
文献类型:
--
作者:
Grebe, Alena;Latz, Eicke

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慢性血管炎症被认为在心血管疾病中具有关键作用。然而,这种炎症反应的诱导剂在血管壁目前还没有得到很好的理解。过量的胆固醇是哺乳动物细胞中丰富的基本脂质分子,可引发动脉粥样硬化的发展和进展。胆固醇在早期动脉粥样硬化病变中的积累导致巨噬细胞泡沫细胞的形成,并且结晶胆固醇被发现是晚期动脉粥样硬化斑块的标志。胆固醇晶体可以激活先天免疫系统的多分子信号传导复合物,NLRP 3炎性体,导致半胱天冬酶-1介导的促炎性白细胞介素-1家族细胞因子的激活和分泌。此外,结晶胆固醇被认为通过物理破坏覆盖动脉粥样硬化病变的纤维帽而诱导斑块破裂。本文就胆固醇沉积和结晶在心血管疾病炎症反应中的作用进行综述。
Chronic vascular inflammation is regarded to have a key role in cardiovascular disease. However, the elicitors of this inflammatory response in the vessel wall are currently not well understood. Excessive amounts of cholesterol, an abundant and fundamental lipid molecule in mammalian cells, can trigger the development and progression of atherosclerosis. Accumulation of cholesterol in early atherosclerotic lesions results in the formation of macrophage foam cells, and crystalline cholesterol is found as a hallmark of advanced atherosclerotic plaques. Cholesterol crystals can activate a multimolecular signaling complex of the innate immune system, the NLRP3 inflammasome, resulting in a caspase-1 mediated activation and secretion of proinflammatory interleukin-1 family cytokines. Furthermore, crystalline cholesterol is thought to induce plaque rupture by physical disruption of the fibrous cap covering atherosclerotic lesions. Here we review the role of cholesterol deposition and crystallization for inflammatory responses in cardiovascular diseases.
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