Role of NLRP3 Inflammasomes in Atherosclerosis.
Role of NLRP3 Inflammasomes in Atherosclerosis.
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DOI：
10.5551/jat.rv17001
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发表时间：
2017-05-01
影响因子：
4.4
通讯作者：
Takahashi M
中科院分区：
文献类型：
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作者：
Karasawa T;Takahashi M
伴有巨噬细胞浸润的炎症是动脉粥样硬化的一个重要特征。尽管其机制尚不清楚，但新出现的证据表明，调节caspase-1激活和随后的pro-IL-1β加工的NLRP3炎症小体引发血管壁炎症反应并导致动脉粥样硬化的进展。NLRP3炎症小体被各种危险信号激活，如巨噬细胞中的胆固醇晶体、磷酸钙晶体和氧化低密度脂蛋白，在动脉粥样硬化病变中启动炎症反应。最近的研究进一步阐明了NLRP3炎症小体的调控机制和潜在的治疗药物。在本研究中，我们回顾了目前关于NLRP3炎症小体在动脉粥样硬化发病机制中的作用的知识现状，并讨论了针对NLRP3炎症小体的治疗方法。
Inflammation with macrophage infiltration is a key feature of atherosclerosis. Although the mechanisms had been unclear, emerging evidence unveiled that NLRP3 inflammasomes, which regulate caspase-1 activation and subsequent processing of pro-IL-1β, trigger vascular wall inflammatory responses and lead to progression of atherosclerosis. NLRP3 inflammasomes are activated by various danger signals, such as cholesterol crystals, calcium phosphate crystals, and oxidized low-density lipoprotein in macrophages, to initiate inflammatory responses in the atherosclerotic lesion. Recent studies have further clarified the regulatory mechanisms and the potential therapeutic agents that target NLRP3 inflammasomes. In this study, we reviewed the present state of knowledge on the role of NLRP3 inflammasomes in the pathogenesis of atherosclerosis and discussed the therapeutic approaches that target NLRP3 inflammasomes.