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首页> 外文期刊>Current opinion in lipidology >Lipoprotein-associated phospholipase A(2) and atherosclerosis.
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Lipoprotein-associated phospholipase A(2) and atherosclerosis.

机译：脂蛋白相关的磷脂酶A（2）和动脉粥样硬化。

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PURPOSE OF REVIEW: There is substantial data from over 50 000 patients that increased lipoprotein-associated phospholipase A2 (Lp-PLA2) mass or activity is associated with an increased risk of cardiac death, myocardial infarction, acute coronary syndromes and ischemic stroke. However, only recently have data emerged demonstrating a role of Lp-PLA2 in development of advanced coronary artery disease. Indeed, Lp-PLA2 may be an important link between lipid homeostasis and the vascular inflammatory response. RECENT FINDINGS: Lp-PLA2, also known as platelet-activating factor acetylhydrolase, rapidly cleaves oxidized phosphatidylcholine molecules produced during the oxidation of LDL and atherogenic lipoprotein Lp(a), generating the soluble proinflammatory and proapoptotic lipid mediators, lyso-phosphatidylcholine and oxidized nonesterified fatty acids. These proinflammatory lipids play an important role in the development of atherosclerotic necrotic cores, the substrate for acute unstable coronary disease by recruiting and activating leukocytes/macrophages, inducing apoptosis and impairing the subsequent removal of dead cells. Selective inhibition of Lp-PLA2 reduces development of necrotic cores and may result in stabilization of atherosclerotic plaques. SUMMARY: Recent data have shown that immune pathways play a major role in the development and progression of high-risk atherosclerosis, which leads to ischemic sudden death, myocardial infarction, acute coronary syndromes and ischemic strokes. Persistent and sustained macrophage apoptosis appears to play a major role in the resulting local inflammatory response in part by effects elicited by Lp-PLA2. Selective inhibition of Lp-PLA2 has been postulated to reduce necrotic core progression and the clinical sequelae of advanced, unstable atherosclerosis.
机译：审查的目的：来自5万多名患者的大量数据表明，脂蛋白相关磷脂酶A2（Lp-PLA2）的质量或活性增加与心脏死亡，心肌梗塞，急性冠状动脉综合征和缺血性中风的风险增加相关。然而，直到最近才出现表明Lp-PLA2在晚期冠状动脉疾病发展中的作用的数据。实际上，Lp-PLA2可能是脂质稳态与血管炎性反应之间的重要联系。最近发现：Lp-PLA2，也称为血小板活化因子乙酰水解酶，可迅速裂解LDL和动脉粥样硬化脂蛋白Lp（a）氧化过程中产生的氧化磷脂酰胆碱分子，产生可溶性促炎和促凋亡脂质介质，溶血磷脂酰胆碱和氧化的非酯化脂肪酸。这些促炎性脂质在动脉粥样硬化坏死核心的发展中起着重要作用，该动脉粥样硬化坏死核心是通过招募和激活白细胞/巨噬细胞，诱导细胞凋亡并损害随后死亡细胞的去除而成为急性不稳定冠状动脉疾病的基质。 Lp-PLA2的选择性抑制可减少坏死核心的形成，并可能导致动脉粥样硬化斑块的稳定。摘要：最新数据表明，免疫途径在高危动脉粥样硬化的发生和发展中起主要作用，导致缺血性猝死，心肌梗塞，急性冠脉综合征和缺血性中风。持久和持续的巨噬细胞凋亡似乎在局部炎症反应中起主要作用，部分是由Lp-PLA2引起的。据推测，Lp-PLA2的选择性抑制作用可减少坏死性核心进程和晚期，不稳定动脉粥样硬化的临床后遗症。

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