METABOLIC SYSTEM OF CHOLESTEROL ELIMINATION FROM TISSUES. POSSIBILITY OF ACTIVATION ITS KEY PARTS
https://doi.org/10.20996/1819-6446-2006-2-2-49-56
Abstract
Lipid metabolism issues are reviewed. Ways of cholesterol transformation are represented thoroughly; proteins regulating its transportation are described. Important place takes the role of high density lipoproteins in backward transportation of cholesterol from peripheral tissues. Possibilities of pharmacological activation of this system, aimed at prevention and treatment of atherosclerosis are discussed.
About the Authors
N. V. PerovaRussian Federation
I. N. Ozerova
Russian Federation
V. A. Metelskaya
Russian Federation
References
1. Tall AK. An overview of reverse cholesterol transport. Eur Heart J 1998; 19:A31-A35.
2. Stein O, Stein Y. Lipid transfer proteins (LTP) and atherosclerosis. Atherosclerosis 2005; 178: 217-230.
3. Rodriguez A, Usher DC. Anti-atherogenic effects of the acylCoA:cholesterol acyltransferase inhibitor, avasimibe (CI-1011), in cultured primary human macrophages. Atherosclerosis 2002; 161(1): 45-54.
4. Bocan TM, Krause BR, Rosebury WS, et al. The combined effect of inhibition both AСAT and HMG-CoA reductase may directly induce atherosclerotic lesion regression. Atherosclerosis 2001; 157 (1): 97- 105.
5. de Medina P, Payre BL, Bernard J, et al. Tamoxifen is a potent inhibitor of cholesterol esterification and prevents the formation of foam cells. J Pharmacol Exp Ther. 2004; 3008 (3): 1165-1173.
6. Sugimoto K, Tsujita M, Wu CA, et al. An inhibitor of acyltransferase increases expression of ATP-binding cassette transporter A1 and thereby enhances the Apo-A1-mediated release of cholesterol from macrophages. Biochim Biophys Acta 2004; 1636 (1): 69-76.
7. Yancey PG, Bornick AE, Kellner-Weibel G, et al. Importance of different pathway of cellular cholesterol efflux. Arterioscler Thromb Vasc Biol. 2003; 23: 712-719.
8. Mendez AJ. Cholesterol efflux mediated by apolipoproteins is an active cellular process distinct from efflux mediated by passive diffusion. J Lipid Res. 1997; 38: 1807-1821.
9. Chambenoit O, Hamon Y, Marguet D, et al. Specific docking of apolipoprotein A1 at the cell surface requires a functional ABCA1 transporter. J Biol Chem. 2001; 276: 9955-9960.
10. Drobnik W, Borsukova H, Bottcher A, et al. Apo A1/ABCA1- dependent and HDL3-mediated lipid efflux from compositionally distinct cholesterol-based microdomains. Traffic 2002; 3: 268-278.
11. Glomset JA. The plasma lecithins:cholesterol acyltransferase reaction. J Lipid Res. 1968; 9: 155-167.
12. Ikewaki K, Matsunaga A, Han H, et al. A novel two nucleotide deletion in the apolipoprotein AI gene, apo AI Shinbashi, associated with HDL deficiency, corneal opacities, planar xantomas, and premature coronary artery disease. Atherosclerosis 2004; 172: 39-45.
13. Forte TM, Subbanagounder G, Berliner JA, et al. Altered activities of anti-atherogenic enzymes LCAT, paraoxonaze, and platelet-activating factor acetylhydrolase in atherosclerosis-susceptible mice. J Lipid Res. 2002; 43: 477-485.
14. Foger B, Chase M, Amar MJ, et al. Cholesteryl ester transfer protein corrects dysfunctional HDLs and reduces aortic atherosclerosis in LCAT transgenic mice. J Biol Chem. 1999; 274 (52): 36912- 36920.
15. Fielding CJ, Fielding PE. Molecular physiology of reverse cholesterol transport. J Lipid Res.1995; 36:211-228.
16. Huang Z, Inazu A, Nohara A, et al. Cholesteryl ester transfer protein inhibitor (JTT-705) and the development of atherosclerosis in rabbits with severe hypercholesterolaemia. Clin Sci (Lond) 2002; 103 (6): 587-594.
17. Clark RW, Sutfin TA, Ruggerri RB, et al. Raising HDL in humans through inhibition of cholesteryl ester transfer protein: an initial multidose study of torsetrapib. Arterioscler Thromb Vasc Biol. 2004; 24: 1-9.
18. Brousseau ME, Schaefer EJ, Wolfe ML, et al. Effects of an inhibitor of cholesteryl ester transfer protein on HDL cholesterol. N Engl J Med. 2004; 350: 1505-1515.
19. Oram JF, Wolfbauer G, Vaughan AM, et al. Phospholipid transfer protein interacts with and stabilizes ATP-binding cassette transporter A1 and enhances cholesterol efflux from cells. J Biol Chem. 2003; 278 (52): 52379-52385.
20. Dullaart RP, van Tol A. Role of phospholipid transfer protein and prebeta HDL in maintaining cholesterol efflux from Fu5AH cells to plasma from insulin-resistant subjects. Scand J Clin Lab Invest. 2001; 61 (1): 69-74.
21. Lie J, De Crom R, van Gent T, et al. Elevation of plasma phospholipid transfer protein increases the risk of atherosclerosis in spite of lowering apolipoprotein B containing lipoproteins. J Lipid Res. 2004; 45 (5): 805-811.
22. Acton S, Rigotti A, Landschulz KT, et al. Identification of scavenger receptor SR-BI as a high density lipoprotein receptor. Science 1996; 271: 518-520.
23. Plump AS, Erickson SK, Weng W, et al. Apo AI is required for cholesterol ester accumulation in steriodogenic celles and for normal adrenal steroid production. J Clin Invest.1996; 97: 2660-2671.
24. Zhao SP, Wu ZH, Hong SC, et al. Effect of atorvastatin on SR-B1 expression and HDL-induced cholesterol efflux in adipocytes of hypercholesterolemic rabbits. Clin Chim Acta 2006; 365 (1-2): 119-124.
25. Семенова Ю.Э., Марцевич С.Ю., Перова Н.В. и др. Оценка эффективности и безопасности дженерика аторвастатина у больных с гиперлипидемией. Рацион Фармакотерап в Кардиол. 2005; 3: 24-28.
Review
For citations:
Perova N.V., Ozerova I.N., Metelskaya V.A. METABOLIC SYSTEM OF CHOLESTEROL ELIMINATION FROM TISSUES. POSSIBILITY OF ACTIVATION ITS KEY PARTS. Rational Pharmacotherapy in Cardiology. 2006;2(2):49-56. (In Russ.) https://doi.org/10.20996/1819-6446-2006-2-2-49-56