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首页> 外文期刊>Rejuvenation Research >Age-Associated Decrease of High-Density Lipoprotein-Mediated Reverse Cholesterol Transport Activity
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Age-Associated Decrease of High-Density Lipoprotein-Mediated Reverse Cholesterol Transport Activity

机译：与年龄相关的高密度脂蛋白介导的胆固醇逆向转运活性降低

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High-density lipoproteins (HDL) are considered atheroprotective in contrast to low-density lipoproteins (LDL), which are atherogenic in their oxidized form. A growing body of evidence suggests that HDL exert part of their antiatherogenic effect by counteracting LDL oxidation as well as their proinflammatory effect. However, a number of studies, carried over the past 30 years, have shown that cholesterol efflux plays a major role in the atheroprotective effects of HDL and cholesterol homeostasis. These studies have further identified the scavenger receptor type B-I (SR-BI), the adenosine triphosphate (ATP)-binding cassette transporters ATP-binding cassette subfamily A1 (ABCA1), ATP-binding cassette subfamily G1 (ABCG1) and ABCG4, the liver X receptor/retinoid X receptor (LXR/RXR) and peroxisome proliferator-activated receptorγ(PPAR γ) transcription factors, the HDL components apolipoprotein A-I (apoA-I), lecithin-cholesterol acyltransferase (LCAT), and phospholipids as additional mediators of cholesterol transport. Cholesterol efflux occurs via three independent pathways: (1) aqueous diffusion, (2) nonspecific efflux via SR-BI receptors, and (3) specific efflux via cholesterol-responsive members of the ABC superfamily. Whereas aqueous diffusion and scavenger receptor class B, type I (SR-BI)-mediated efflux transport free cholesterol to a wide variety of cholesterol acceptors (particles containing phospholipids, HDL, and lipidated apo-lipoproteins; LDL, etc), the ABCA1 pathway mediates the transport of cholesterol in a unidirectional manner, mainly to lipid-poor apoA-I. In contrast, the ABCG1 pathway is responsible for the transport of cholesterol to all the subfamily members of HDL. Although HDL-mediated cholesterol efflux is apoA-I-dependent, recent studies have suggested an involvement of the enzyme paraoxonase 1 (PON1). Cholesterol efflux is carried on by a number of factors such as genetic mutations, smoking, stress, and high-fat diets. It is attenuated with aging due to changes in the composition and structure of HDL, especially the phosphatidylcholine/sphingomyelin ratio, the fluidity of the phospholipidic layer, the concentration of apoA-I, and the activity of PON1. This review summarizes the findings that cholesterol homeostasis is disrupted with aging as a consequence of dysfunctional cholesterol efflux and the impairment of physiological functions.
机译：与低密度脂蛋白（LDL）以氧化形式发生动脉粥样硬化相比，高密度脂蛋白（HDL）被认为具有抗动脉粥样硬化作用。越来越多的证据表明，HDL通过抵消LDL氧化及其促炎作用而发挥其部分抗动脉粥样硬化作用。然而，过去30年进行的许多研究表明，胆固醇外排在HDL和胆固醇体内平衡的抗动脉粥样硬化作用中起着重要作用。这些研究进一步确定了清道夫受体型BI（SR-BI），三磷酸腺苷（ATP）结合盒转运蛋白ATP结合盒亚家族A1（ABCA1），ATP结合盒亚家族G1（ABCG1）和ABCG4，肝脏X受体/类视黄醇X受体（LXR / RXR）和过氧化物酶体增殖物激活受体γ（PPARγ）转录因子，HDL成分载脂蛋白AI（apoA-I），卵磷脂-胆固醇酰基转移酶（LCAT）和磷脂作为胆固醇的其他介体运输。胆固醇外排通过三个独立的途径发生：（1）水扩散，（2）通过SR-BI受体的非特异性外排，和（3）通过ABC超家族的胆固醇反应性成员的特异性外排。而B型水扩散和清除剂受体，I型（SR-BI）介导的外排将游离胆固醇转运至多种胆固醇受体（含有磷脂，HDL和脂化载脂蛋白的颗粒； LDL等），ABCA1途径以单向方式介导胆固醇的运输，主要是向贫脂的apoA-I。相反，ABCG1途径负责胆固醇向HDL的所有亚家族成员的转运。尽管HDL介导的胆固醇外排是apoA-I依赖性的，但最近的研究表明该酶涉及对氧磷过氧化物酶1（PON1）。胆固醇外排受多种因素影响，例如基因突变，吸烟，压力和高脂饮食。由于HDL的组成和结构的变化，尤其是磷脂酰胆碱/鞘磷脂的比率，磷脂层的流动性，apoA-I的浓度以及PON1的活性的变化，其随着衰老而衰减。这项综述总结了以下发现：由于胆固醇外排功能障碍和生理功能受损，胆固醇的体内平衡会随着衰老而被破坏。

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  • 来源
    《Rejuvenation Research》 |2009年第2期|117-126|共10页
  • 作者

    Hicham Berrougui; Abdelouahed Khalil;

  • 作者单位

    Research Center on Aging, Sherbrooke University Geriatric Institute, Sherbrooke, Quebec, Canada.|Geriatrics Service, Department of Medicine, Université de Sherbrooke, Sherbrooke, Quebec, Canada.;

    Research Center on Aging, Sherbrooke University Geriatric Institute, Sherbrooke, Quebec, Canada.|Geriatrics Service, Department of Medicine, Université de Sherbrooke, Sherbrooke, Quebec, Canada.;

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