Infection and inflammation-induced proatherogenic changes of lipoproteins
Infection and inflammation-induced proatherogenic changes of lipoproteins
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DOI：
10.1086/315611
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发表时间：
2000-06-01
影响因子：
6.4
通讯作者：
Grunfeld, C
中科院分区：
文献类型：
--
作者：
Khovidhunkit, W;Memon, RA;Grunfeld, C
流行病学研究表明感染/炎症和动脉粥样硬化之间存在联系。在对感染和炎症的急性期反应期间，细胞因子诱导导致脂蛋白变化的组织和血浆事件。这些变化中有许多与促进动脉粥样硬化形成的变化相似。本文综述了脂蛋白在感染和炎症过程中的变化，重点介绍了那些可能导致动脉粥样硬化的脂蛋白。高甘油三酯血症、富含甘油三酯的脂蛋白升高、小而密的低密度脂蛋白的出现、血小板活化因子乙酰水解酶活性升高、分泌型磷脂酶A（2）、鞘脂富集脂蛋白和高密度脂蛋白胆固醇降低都是可促进动脉粥样硬化形成的变化。此外，与HDL代谢相关的蛋白质的改变（例如，对氧磷酶、载脂蛋白A-T、卵磷脂：胆固醇酰基转移酶、胆固醇。酯转移蛋白、肝脂酶、磷脂转移蛋白和血清淀粉样蛋白A）可通过抗氧化和逆转胆固醇转运机制降低HDL对抗动脉粥样硬化形成的能力。脂蛋白的这些致动脉粥样硬化的变化可能有助于感染/炎症和动脉粥样硬化之间的联系。
Epidemiologic studies suggest a link between infection/inflammation and atherosclerosis. During the acute-phase response to infection and inflammation, cytokines induce tissue and plasma events that lead to changes in lipoprotein. Many of these changes are similar to those proposed to promote atherogenesis. The changes of lipoproteins during infection and inflammation are reviewed with a focus on those that are potentially proatherogenic. Hypertriglyceridemia, elevated triglyceride-rich lipoproteins, the appearance of small dense low-density lipoproteins, increased platelet-activating factor acetylhydrolase activity, and secretory phospholipase A(2), sphingolipid-enriched lipoproteins, and decreased high-density lipoprotein (HDL) cholesterol are changes that could promote atherogenesis. Moreover, alterations of proteins associated with HDL metabolism (e.g., paraoxonase, apolipoprotein A-T, lecithin:cholesterol acyltransferase, cholesterol. ester transfer protein, hepatic lipase, phospholipid transfer protein, and serum amyloid A) could decrease the ability of HDL to protect against atherogenesis through antioxidation and reverse cholesterol transport mechanisms. These proatherogenic changes of Lipoproteins may contribute to the link between infection/inflammation and atherosclerosis.