Journals / The Anatolian Journal of Cardiology / 2017 / Cilt: 18 - Sayı: 2

High-density lipoprotein metabolism and reverse cholesterol transport: strategies for raising HDL cholesterol

Pages
149–154
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Results of clinical trials should be awaited before further clinical management of atherosclerotic cardiovascular disease

📌 3 Key Takeaways

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Objective & Hypothesis:A key to effective treatment of cardiovascular disease is to understand the body’s complex lipoprotein transport system.
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Key Findings & Data:HDL heterogeneity is the result of the activity of several factors that assemble and remodel HDL particles in plasma: ATP-binding cassette transporter A1 (ABCA1), lecithin cholesterol acyltransferase (LCAT), cholesteryl ester transfer protein (CETP), hepatic lipase (HL), phospholipid transfer protein (PLTP), endothelial lipase (EL), and scavenger receptor class B type I (SR-BI).
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Conclusion & Impact:Results of clinical trials should be awaited before further clinical management of atherosclerotic cardiovascular disease
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

A key to effective treatment of cardiovascular disease is to understand the body’s complex lipoprotein transport system. Reverse cholesterol transport (RCT) is the process of cholesterol movement from the extrahepatic tissues back to the liver. Lipoproteins containing apoA-I [highdensity lipoprotein (HDL)] are key mediators in RCT, whereas non-high-density lipoproteins (non-HDL, lipoproteins containing apoB) are involved in the lipid delivery pathway. HDL particles are heterogeneous; they differ in proportion of proteins and lipids, size, shape, and charge. HDL heterogeneity is the result of the activity of several factors that assemble and remodel HDL particles in plasma: ATP-binding cassette transporter A1 (ABCA1), lecithin cholesterol acyltransferase (LCAT), cholesteryl ester transfer protein (CETP), hepatic lipase (HL), phospholipid transfer protein (PLTP), endothelial lipase (EL), and scavenger receptor class B type I (SR-BI). The RCT pathway consists of the following steps: 1. Cholesterol efflux from peripheral tissues to plasma, 2. LCAT-mediated esterification of cholesterol and remodeling of HDL particles, 3. direct pathway of HDL cholesterol delivery to the liver, and 4. indirect pathway of HDL cholesterol delivery to the liver via CETP-mediated transfer There are several established strategies for raising HDL cholesterol in humans, such as lifestyle changes; use of drugs including fibrates, statins, and niacin; and new therapeutic approaches. The therapeutic approaches include CETP inhibition, peroxisome proliferator-activated receptor (PPAR) agonists, synthetic farnesoid X receptor agonists, and gene therapy. Results of clinical trials should be awaited before further clinical management of atherosclerotic cardiovascular disease

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Cite This Article

TRAJKOVSKA, K. T., TOPUZOVSKA, S. (2017). High-density lipoprotein metabolism and reverse cholesterol transport: strategies for raising HDL cholesterol. The Anatolian Journal of Cardiology, Cilt: 18 - Sayı: 2, 149–154. https://ajindex.com/articles/366813

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References (17)

  1. Smith LC, Pownall HJ, Gotto AM Jr. The plasma lipoproteins: structure and metabolism. Annu Rev Biochem 1978; 47: 751-7
  2. Libby P. Inflammation in atherosclerosis. Nature 2002; 420: 868-74
  3. Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med 2005; 352: 1685-95
  4. Castelli WP, Anderson K, Wilson PW, Levy D. Lipids and risk of coronary heart disease. The Framingham Study. Ann Epidemiol 1992; 2: 23-8
  5. Lusis AJ, Fogelman AM, Fonarow GC. Genetic basis of atherosclerosis: part I: new genes and pathways. Circulation 2004;110: 1868-73
  6. Franceschini G. Apolipoprotein function in health and disease: insights from natural mutations. Eur J Clin Invest 1996; 26: 733-46
  7. Fielding CJ, Fielding PE. Molecular physiology of reverse cholesterol transport. J Lipid Res 1995; 36: 211-228. 8. van der Velde AE. Reverse cholesterol transport: from classical view to new insights. World J Gastroenterol 2010; 16: 5908-15
  8. Welty FK, Lichtenstein AH, Barrett PH, Dolnikowski GG, Schaefer EJ. Interrelationships between human apolipoprotein A-I and apolipoproteins B-48 and B-100 kinetics using stable isotopes. Arterioscler Thromb Vasc Biol 2004; 24: 1703-7
  9. Ramjee V, Sperling LS, Jacobson TA. Non-high-density lipoprotein cholesterol versus apolipoprotein B in cardiovascular risk stratification: do the math. J Am Coll Cardiol 2011; 58: 457-63
  10. Barter P. HDL-C: Role as a risk modifier. Atheroscler Suppl 2011; 12: 267-70
  11. Havel RJ. Postprandial lipid metabolism: an overview. Proc Nutr Soc 1997; 56: 659-66
  12. Navab M, Hama SY, Hough GP, Hedrick CC, Sorenson R, La Du BN, et al. High density associated enzymes: their role in vascular biology. Curr Opin Lipidol 1998; 9: 449-56
  13. Goldberg IJ, Blaner WS, Vanni TM, Moukides M, Ramakrishnan R. Role of lipoprotein lipase in the regulation of high density lipoprotein apolipoprotein metabolism. Studies in normal and lipoprotein lipase-inhibited monkeys. J Clin Invest 1990; 86: 463-73
  14. Fazio S, Pamir N. HDL particle size and functional heterogeneity. Circ Res 2016; 119: 704-7
  15. Rached FH, Chapman MJ, Kontush A. HDL particle subpopulations: Focus on biological function. Biofactors 2015; 41: 67-77
  16. Barter PJ. Hugh sinclair lecture: the regulation and remodeling of HDL by plasma factors. Atheroscler Suppl 2002; 3: 39-47
  17. Kontush A, Lindahl M, Lhomme M, Calabresi L, Chapman MJ, Davidson WS. Structure of HDL: particle subclasses and molecular components. Handb Exp Pharmacol