Kontush Anatol, Chapman M John
National Institute for Health and Medical Research (INSERM), Unité 551, Hôpital de la Pitié, Paris, France.
Nat Clin Pract Cardiovasc Med. 2006 Mar;3(3):144-53. doi: 10.1038/ncpcardio0500.
Our understanding of the relationship between the atheroprotective activities of HDL and heterogeneity of HDL particles has advanced greatly. HDL particles are highly heterogeneous in structure, intravascular metabolism and antiatherogenic activity. In this review, we discuss new findings on the antiatherogenic properties of HDL particles. Small, dense HDL possesses potent antioxidative activity but this is compromised under conditions of atherogenic dyslipidemia. HDL functional deficiency frequently coincides with reductions in HDL-cholesterol concentration and alterations in HDL metabolism and structure. Formation of small, dense HDL particles with attenuated antiatherogenic activity can be mechanistically related to HDL enrichment in triglycerides and in serum amyloid A, depletion of cholesteryl esters, covalent modification of HDL apolipoproteins and attenuated antiatherogenic function of apolipoprotein AI. Low circulating levels of HDL cholesterol might, therefore, be associated with the defective functionality of small HDL particles of abnormal structure and composition. In common metabolic diseases, such as type 2 diabetes and metabolic syndrome, deficiency of HDL particle number and function favor accelerated atherosclerosis. Therapeutic normalization of the quantity, quality and biological activities of HDL particles thus represents a novel approach to attenuating atherosclerosis in dyslipidemic individuals with metabolic disease. Cholesteryl ester transfer protein inhibitors, nicotinic acid, reconstituted HDL and other HDL-raising agents are being investigated. Induction of selective increase in the circulating concentrations of small, dense HDL3 particles with increased antiatherogenic activity seems especially promising, particularly for therapy of atherogenic dyslipidemia.
我们对高密度脂蛋白(HDL)的抗动脉粥样硬化活性与HDL颗粒异质性之间关系的理解有了很大进展。HDL颗粒在结构、血管内代谢和抗动脉粥样硬化活性方面具有高度异质性。在这篇综述中,我们讨论了HDL颗粒抗动脉粥样硬化特性的新发现。小而密的HDL具有强大的抗氧化活性,但在动脉粥样硬化性血脂异常的情况下,这种活性会受到损害。HDL功能缺陷常与HDL胆固醇浓度降低以及HDL代谢和结构改变同时出现。具有减弱抗动脉粥样硬化活性的小而密HDL颗粒的形成,在机制上可能与HDL中甘油三酯和血清淀粉样蛋白A的富集、胆固醇酯的消耗、HDL载脂蛋白的共价修饰以及载脂蛋白AI抗动脉粥样硬化功能的减弱有关。因此,循环中HDL胆固醇水平低可能与结构和组成异常的小HDL颗粒功能缺陷有关。在常见的代谢性疾病,如2型糖尿病和代谢综合征中,HDL颗粒数量和功能的缺乏有利于动脉粥样硬化的加速发展。因此,对HDL颗粒的数量、质量和生物活性进行治疗性正常化,代表了一种在患有代谢性疾病的血脂异常个体中减轻动脉粥样硬化的新方法。胆固醇酯转运蛋白抑制剂、烟酸、重组HDL和其他升高HDL的药物正在研究中。诱导具有增强抗动脉粥样硬化活性的小而密HDL3颗粒的循环浓度选择性增加似乎特别有前景,尤其是对于动脉粥样硬化性血脂异常的治疗。