Cholesterol crystals piercing the arterial plaque and intima trigger local and systemic inflammation
Cholesterol crystals piercing the arterial plaque and intima trigger local and systemic inflammation
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DOI：
10.1016/j.jacl.2010.03.003
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发表时间：
2010-06-01
影响因子：
4.4
通讯作者：
Abela, George S.
中科院分区：
文献类型：
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作者：
Abela, George S.
对动脉壁损伤的反应是一个炎症过程。随着时间的推移，它成为动脉粥样硬化和随后斑块不稳定性发展的组成部分。对这一过程至关重要的潜在有害因素尚未受到太多关注。在这篇综述中，假设斑块破裂模型分为两个阶段：（胆固醇晶体诱导的细胞损伤和凋亡），细胞内胆固醇晶体诱导壤土细胞凋亡，通过向更多的巨噬细胞发出信号建立恶性循环，导致细胞外脂质的积聚这种局部炎症最终导致易损斑块的半液体、富含脂质的坏死核心的形成。（胆固醇结晶诱导的动脉壁损伤），饱和脂质核心现在准备结晶，这可以表现为具有全身炎症反应的临床综合征。胆固醇结晶是引起核心膨胀的触发因素。导致内膜损伤我们最近证明，当胆固醇从液态结晶成固态时，它经历体积膨胀。其可以撕裂斑块帽。在死于急性冠状动脉综合征的患者的斑块中观察到胆固醇晶体穿透帽和内膜表面。他汀类药物、阿司匹林和乙醇）可以溶解胆固醇晶体，并且可以通过这种直接机制发挥它们的直接益处。此外，因为最近的研究已经证明，在选择他汀类药物治疗的患者中，C-反应蛋白可以是可靠的标志物，所以它可以反映胆固醇晶体引起的内膜损伤的存在。这在动脉粥样硬化兔模型中得到了证明。因此，我们认为胆固醇结晶可以部分解释与动脉粥样硬化相关的局部和全身炎症（C）2010国家脂质协会保留所有权利
The response to arterial wall injury is an inflammatory process. which over time becomes Integral to the development of atherosclerosis and subsequent plaque instability However. the underlying injurious agent, critical to this process, has not received much attention In this review, a model of plaque rupture is hypothesized with two stages of in activity In stage I (cholesterol crystal-induced cell injury and apoptosis), intracellular cholesterol crystals induce loam cell apoptosis, setting up a vicious cycle by signaling more macrophages, resulting in accumulation of extra cellular lipids This local inflammation eventually leads to the formation of a semi-liquid, lipid-rich necrotic core of a vulnerable plaque In stage II (cholesterol crystal-induced arterial wall injury), the saturated lipid core is now primed for crystallization, which can manifest as a clinical syndrome with a systemic inflammation response Cholesterol crystallization is the trigger that causes core expansion. leading to intimal injury We recently demonstrated that when cholesterol crystallizes from a liquid to a solid state, it undergoes volume expansion. which can tear the plaque cap This observation of cholesterol crystals perforating the cap and intimal surface was made in the plaques of patients who died with acute coronary syndrome We have also demonstrated that several agents (ie. statins, aspirin, and ethanol) can dissolve cholesterol crystals and may be exerting their immediate benefits by this direct mechanism Also, because recent studies have demonstrated that It C-reactive protein may be a reliable marker in selecting patients for statin therapy, it could reflect the presence of intimal injury by cholesterol crystals This was demonstrated in an atherosclerotic rabbit model Therefore, we propose that cholesterol crystallization could help explain in part both local and systemic inflammation associated with atherosclerosis (C) 2010 National Lipid Association All rights reserved