Speciated High-Density Lipoprotein Biogenesis and Functionality.
نویسندگان
چکیده
Plasma high-density lipoprotein cholesterol (HDL-C) concentration is a negative risk factor for atherosclerotic cardiovascular disease (CVD). Despite this, most attempts to raise plasma HDL-C concentrations in a cardioprotective way have failed. Recently, hypotheses about the atheroprotective effects of HDL have shifted away from quantity to quality, mostly HDL function in reverse cholesterol transport. Plasma HDL from CVD patients is a poorer acceptor of cellular cholesterol than plasma from healthy controls, independent of plasma HDL-C concentrations. The function of HDL is likely determined by two other factors, stability and composition. The kinetic instability of HDL, which varies according to subclass, is a likely determinant of its reactivity in response to many HDL-modifying activities. HDL composition is also heterogeneous and variable; all HDL particles contain apo AI but only about two-thirds contain apo AII. This occurs despite the fact that apo AI and apo AII are hepatically secreted on separate HDL that later fuse in plasma. HDL also contains traces of other proteins, some of which have not yet been associated with HDL function. One minor HDL species are those that are secreted with intact signal peptides, which enhances their binding to HDL; these HDL have special properties that are independent of cholesterol transport. Here, we review and provide a perspective about what is currently known about speciated HDL biogenesis in the context of health and disease.
منابع مشابه
A novel compound inhibits reconstituted high-density lipoprotein assembly and blocks nascent high-density lipoprotein biogenesis downstream of apolipoprotein AI binding to ATP-binding cassette transporter A1-expressing cells.
OBJECTIVE Nascent high-density lipoprotein (HDL) particles form from cellular lipids and extracellular lipid-free apolipoprotein AI (apoAI) in a process mediated by ATP-binding cassette transporter A1 (ABCA1). We have sought out compounds that inhibit nascent HDL biogenesis without affecting ABCA1 activity. METHODS AND RESULTS Reconstituted HDL (rHDL) formation and cellular cholesterol efflux...
متن کاملApolipoprotein AI Binding to ATP-Binding Cassette Transporter A1 and Blocks Nascent High-Density Lipoprotein Biogenesis Downstream of A Novel Compound Inhibits Reconstituted High-Density Lipoprotein Assembly
Cells Expressing − Apolipoprotein AI Binding to ATP-Binding Cassette Transporter A1 and Blocks Nascent High-Density Lipoprotein Biogenesis Downstream of A Novel Compound Inhibits Reconstituted High-Density Lipoprotein Assembly ISSN: 1524-4636 Copyright © 2011 American Heart Association. All rights reserved. Print ISSN: 1079-5642. Online 7272 Greenville Avenue, Dallas, TX 72514 Arteriosclerosis,...
متن کاملPlasma lipoproteins in normal and preeclamptic pregnant women
Background: Preeclampsia is one of the most common complications of pregnancy. It is the cause of high morbidity and mortality for mothers and fetuses, especially in developing countries. The etiology of preeclampsia is unknown. One of the hypothesis on pathophysiology of preeclampsia is dyslipidemia. The aim of this study was to determine maternal plasma levels of lipoproteins in patients with...
متن کاملMicroRNA control of high-density lipoprotein metabolism and function.
Recent discoveries of microRNAs (miRNAs) that control high-density lipoprotein abundance and function have expanded our knowledge of the mechanisms regulating this important lipoprotein subclass. miRNAs have been shown to regulate gene networks that control high-density lipoprotein biogenesis and uptake, as well as discrete steps in the reverse cholesterol transport pathway. Furthermore, high-d...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Current atherosclerosis reports
دوره 18 5 شماره
صفحات -
تاریخ انتشار 2016