Brewer H Bryan
Molecular Disease Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md 20892, USA.
Am Heart J. 2004 Jul;148(1 Suppl):S14-8. doi: 10.1016/j.ahj.2004.04.027.
Low high-density lipoprotein (HDL) cholesterol is associated with increased risk of coronary heart disease (CHD). Ongoing investigation into the mechanisms whereby HDL cholesterol might provide protection from atherosclerosis and clinical disease has resulted in improved understanding of the role of HDL in removal of cholesterol from the arterial wall and has suggested a number of strategies for augmenting the beneficial activities of the lipoprotein. Current drug options for increasing HDL cholesterol levels include the statins, fibrates, and niacin. Strategies in development for increasing the function of HDL or apolipoprotein A-I and thereby reducing atherosclerotic progression include use of agents to upregulate the adenosine triphosphate-binding cassette transporter in vessel wall macrophages to increase cholesterol efflux from these cells; use of agents to stimulate endogenous apoA-I synthesis; administration of apoA-I, apoA-I Milano, apoA-I-mimetic peptides, or delipidated HDL; and use of cholesteryl ester transfer protein inhibitors.
低高密度脂蛋白（HDL）胆固醇与冠心病（CHD）风险增加相关。对HDL胆固醇可能提供抗动脉粥样硬化和临床疾病保护的机制进行的持续研究，增进了对HDL在从动脉壁清除胆固醇中作用的理解，并提出了一些增强脂蛋白有益活性的策略。目前用于提高HDL胆固醇水平的药物选择包括他汀类药物、贝特类药物和烟酸。正在研发的提高HDL或载脂蛋白A-I功能从而减少动脉粥样硬化进展的策略包括：使用药物上调血管壁巨噬细胞中的三磷酸腺苷结合盒转运体以增加这些细胞的胆固醇流出；使用药物刺激内源性载脂蛋白A-I合成；给予载脂蛋白A-I、载脂蛋白A-I米兰型、载脂蛋白A-I模拟肽或脱脂HDL；以及使用胆固醇酯转运蛋白抑制剂。
