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Therapies to Increase ApoA-I and HDL-Cholesterol Levels

机译：提高ApoA-I和HDL-胆固醇水平的疗法

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Cholesterol is transported around the body in the form of lipoprotein (lipid/protein) complexes, because it is almost insoluble in water. High-density lipoprotein (HDL) particles transport cholesterol from tissues back to the liver for excretion. Epidemiological studies have shown an inverse relationship between blood levels of HDL-cholesterol (HDL-c) and the incidence of clinically signi?cant atherosclerosis. The bene?cial effects of HDL in altering atherosclerotic disease are believed to involve elevated levels of HDL enhancing the ef?ux of cholesterol from arterial walls, increasing transport of cholesterol from arteries to the liver for excretion. This reverse cholesterol transport (RCT) pathway is used to explain both HDL’s role in lipid metabolism and the inverse association between HDL-c plasma concentration and the risk of car- diovascular disease. Based on the RCT model, ApoA-I is an attractive target for therapeutic intervention. Experimental manipulations to increase production of ApoA-I have been associated with reduced atherogenicity. There is a continuing need for novel therapies that increase the biosynthesis of HDL, to inhibit the progression of and even bring about regression of atherosclerosis. Small molecule compounds that increase the production of endogenous ApoA-I would be attractive therapeutic agents for treating dyslipidemias.
机译：胆固醇以脂蛋白（脂质/蛋白质）复合物的形式在体内运输，因为它几乎不溶于水。高密度脂蛋白（HDL）颗粒将胆固醇从组织转运回肝脏进行排泄。流行病学研究表明，血液中的HDL-胆固醇（HDL-c）水平与临床上重要的动脉粥样硬化的发生率成反比。据信HDL在改变动脉粥样硬化疾病中的有益作用包括升高水平的HDL增强了胆固醇从动脉壁的流出，增加了胆固醇从动脉向肝脏排泄的运输。这种反向胆固醇转运（RCT）通路既可以解释HDL在脂质代谢中的作用，又可以解释HDL-c血浆浓度与心血管疾病风险之间的负相关关系。基于RCT模型，ApoA-I是治疗干预的诱人靶标。增加ApoA-I产生的实验操作与动脉粥样硬化性降低有关。持续需要增加HDL生物合成，抑制动脉粥样硬化的进展甚至导致动脉粥样硬化消退的新疗法。增加内源性ApoA-I产生的小分子化合物将是治疗血脂异常的有吸引力的治疗剂。

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