MATURATION OF HIGH-DENSITY LIPOPROTEINS

高密度脂蛋白的成熟

• 批准号: 8172032
• 负责人: AMY SHIH
• 金额: $ 3.35万
• 依托单位: UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-08-01 至 2011-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8172032
• 关键词: Apolipoprotein A-I; Blood Vessel Tissue; Cholesterol; Computer Retrieval of Information on Scientific Projects Database; Coronary heart disease; Esterification; Funding; Grant; High Density Lipoproteins; Institution; Lipids; Lipoproteins; Liver; Pathway interactions; Peripheral; Production; Proteins; Research; Research Personnel; Resources; Risk; Role; Source; Tissues; United States National Institutes of Health; discoidal lipoproteins; particle; reverse cholesterol transport

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. High-density lipoproteins (HDL) (http://www.ks.uiuc.edu/Research/Lipoproteins/) are protein-lipid assemblies involved in the transport of cholesterol from peripheral tissues to the liver for degradation. HDL is often called "good cholesterol" due to its role in removing excess cholesterol from tissues and blood vessels. Lower than average levels of HDL have been implicated in an increased risk of coronary heart disease. The production, transformation, and degradation of HDL is regulated by the reverse cholesterol transport pathway. Apolipoprotein A-I (apo A-I), the primary protein component of HDL, initially forms lipid-free/poor HDL particles. The incorporation of cholesterol and lipids into lipid-free/poor HDL particles causes a structural change, forming discoidal lipoprotein particles. Continued efflux of cholesterol and lipids as well as the esterification of cholesterol results in the transformation of the discoidal particles into mature spherical particles, which transport the cholesterol to the liver [1].

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 高密度脂蛋白（HDL）（http：//www.ks.uiuc.edu/Research/Lipoproteins/）是参与代谢的蛋白质-脂质组装体。 将胆固醇从外周组织转运到肝脏进行降解。HDL通常被称为“好胆固醇”， 它在清除组织和血管中多余的胆固醇方面的作用。 低于平均水平的HDL已经 与冠心病风险增加有关。 HDL的产生、转化和降解是 由胆固醇逆向转运途径调节。载脂蛋白A-I（apo A-I），是肝硬化的主要蛋白质成分， HDL最初形成无脂质/贫HDL颗粒。 胆固醇和脂质掺入无脂质/贫HDL颗粒 引起结构变化，形成盘状脂蛋白颗粒。 胆固醇和脂质的持续流出以及 胆固醇的酯化导致盘状颗粒转化为成熟的球形颗粒， 将胆固醇输送到肝脏[1]。