Skip to main content
Erschienen in: Current Atherosclerosis Reports 3/2011

01.06.2011

Lecithin Cholesterol Acyltransferase: An Anti- or Pro-atherogenic Factor?

verfasst von: Xavier Rousset, Robert Shamburek, Boris Vaisman, Marcelo Amar, Alan T. Remaley

Erschienen in: Current Atherosclerosis Reports | Ausgabe 3/2011

Einloggen, um Zugang zu erhalten

Abstract

Lecithin cholesterol acyl transferase (LCAT) is a plasma enzyme that esterifies cholesterol and raises high-density lipoprotein cholesterol, but its role in atherosclerosis is not clearly established. Studies of various animal models have yielded conflicting results, but studies done in rabbits and non-human primates, which more closely simulate human lipoprotein metabolism, indicate that LCAT is likely atheroprotective. Although suggestive, there are also no biomarker studies that mechanistically link LCAT with cardiovascular disease. Imaging studies of patients with LCAT deficiency have also not yielded a clear answer to the role of LCAT in atherosclerosis. Recombinant LCAT, however, is currently being developed as a therapeutic product for enzyme replacement therapy of patients with genetic disorders of LCAT for the prevention and/or treatment of renal disease, but it may also have value for the treatment of acute coronary syndrome.
Literatur
1.
Zurück zum Zitat Rousset X, Vaisman B, Amar M, Sethi AA, Remaley AT. Lecithin: cholesterol acyltransferase–from biochemistry to role in cardiovascular disease. Curr Opin Endocrinol Diabetes Obes. 2009;16(2):163–71.PubMedCrossRef Rousset X, Vaisman B, Amar M, Sethi AA, Remaley AT. Lecithin: cholesterol acyltransferase–from biochemistry to role in cardiovascular disease. Curr Opin Endocrinol Diabetes Obes. 2009;16(2):163–71.PubMedCrossRef
2.
Zurück zum Zitat Santamarina-Fojo S, Hoeg JM, Assmann G, H. Bryan Brewer J: Lecithin Cholesterol Acyltransferase Deficiency and Fish Eye Disease. In: Metabolic & Molecular Bases of Inherited Disease. 2001. Santamarina-Fojo S, Hoeg JM, Assmann G, H. Bryan Brewer J: Lecithin Cholesterol Acyltransferase Deficiency and Fish Eye Disease. In: Metabolic & Molecular Bases of Inherited Disease. 2001.
3.
Zurück zum Zitat Chang T-Y, Li B-L, Chang CCY, Urano Y. Acyl-coenzyme A: cholesterol acyltransferases. Am J Physiol Endocrinol Metab. 2009;297(1):E1–9.PubMedCrossRef Chang T-Y, Li B-L, Chang CCY, Urano Y. Acyl-coenzyme A: cholesterol acyltransferases. Am J Physiol Endocrinol Metab. 2009;297(1):E1–9.PubMedCrossRef
4.
Zurück zum Zitat Czarnecka H, Yokoyama S. Regulation of cellular cholesterol efflux by lecithin:cholesterol acyltransferase reaction through nonspecific lipid exchange. Journal of Biological Chemistry. 1996;271(4):2023–8.PubMedCrossRef Czarnecka H, Yokoyama S. Regulation of cellular cholesterol efflux by lecithin:cholesterol acyltransferase reaction through nonspecific lipid exchange. Journal of Biological Chemistry. 1996;271(4):2023–8.PubMedCrossRef
5.
Zurück zum Zitat Nofer JR, Remaley A. Tangier disease: still more questions than answers. Cellular and Molecular Life Sciences. 2005;62(19):2150–60.PubMedCrossRef Nofer JR, Remaley A. Tangier disease: still more questions than answers. Cellular and Molecular Life Sciences. 2005;62(19):2150–60.PubMedCrossRef
6.
Zurück zum Zitat Yvan-Charvet L, Kling J, Pagler T, et al. Cholesterol efflux potential and antiinflammatory properties of high-density lipoprotein after treatment with niacin or anacetrapib. Arterioscl Throm Vas. 2010;30(7):1430–U1405.CrossRef Yvan-Charvet L, Kling J, Pagler T, et al. Cholesterol efflux potential and antiinflammatory properties of high-density lipoprotein after treatment with niacin or anacetrapib. Arterioscl Throm Vas. 2010;30(7):1430–U1405.CrossRef
7.
Zurück zum Zitat Nishiwaki M, Ikewaki K, Bader G, et al. Human lecithin:cholesterol acyltransferase deficiency: in vivo kinetics of low-density lipoprotein and lipoprotein-X. Arterioscler Thromb Vasc Biol. 2006;26(6):1370–5.PubMedCrossRef Nishiwaki M, Ikewaki K, Bader G, et al. Human lecithin:cholesterol acyltransferase deficiency: in vivo kinetics of low-density lipoprotein and lipoprotein-X. Arterioscler Thromb Vasc Biol. 2006;26(6):1370–5.PubMedCrossRef
8.
Zurück zum Zitat Lynn EG, Choy PC, Magil A. O K: uptake and metabolism of lipoprotein-X in mesangial cells. Mol Cell Biochem. 1997;175(1–2):187–94.PubMedCrossRef Lynn EG, Choy PC, Magil A. O K: uptake and metabolism of lipoprotein-X in mesangial cells. Mol Cell Biochem. 1997;175(1–2):187–94.PubMedCrossRef
9.
Zurück zum Zitat Rader DJ. Lecithin: cholesterol acyltransferase and atherosclerosis: another high-density lipoprotein story that doesn’t quite follow the script. Circulation. 2009;120(7):549–52.PubMedCrossRef Rader DJ. Lecithin: cholesterol acyltransferase and atherosclerosis: another high-density lipoprotein story that doesn’t quite follow the script. Circulation. 2009;120(7):549–52.PubMedCrossRef
10.
Zurück zum Zitat Greeve J, Altkemper I, Dieterich JH, Greten H, Windler E. Apolipoprotein B mRNA editing in 12 different mammalian species: hepatic expression is reflected in low concentrations of apoB-containing plasma lipoproteins. J Lipid Res. 1993;34(8):1367–83.PubMed Greeve J, Altkemper I, Dieterich JH, Greten H, Windler E. Apolipoprotein B mRNA editing in 12 different mammalian species: hepatic expression is reflected in low concentrations of apoB-containing plasma lipoproteins. J Lipid Res. 1993;34(8):1367–83.PubMed
11.
Zurück zum Zitat Paigen B, Ishida BY, Verstuyft J, Winters RB, Albee D. Atherosclerosis susceptibility differences among progenitors of recombinant inbred strains of mice. Arteriosclerosis. 1990;10(2):316–23.PubMed Paigen B, Ishida BY, Verstuyft J, Winters RB, Albee D. Atherosclerosis susceptibility differences among progenitors of recombinant inbred strains of mice. Arteriosclerosis. 1990;10(2):316–23.PubMed
12.
Zurück zum Zitat Berard AM, Foger B, Remaley A, et al. High plasma HDL concentrations associated with enhanced atherosclerosis in transgenic mice overexpressing lecithin-cholesteryl acyltransferase. Nat Med. 1997;3(7):744–9.PubMedCrossRef Berard AM, Foger B, Remaley A, et al. High plasma HDL concentrations associated with enhanced atherosclerosis in transgenic mice overexpressing lecithin-cholesteryl acyltransferase. Nat Med. 1997;3(7):744–9.PubMedCrossRef
13.
Zurück zum Zitat Foger B, Chase M, Amar MJ, et al. Cholesteryl ester transfer protein corrects dysfunctional high density lipoproteins and reduces aortic atherosclerosis in lecithin cholesterol acyltransferase transgenic mice. J Biol Chem. 1999;274(52):36912–20.PubMedCrossRef Foger B, Chase M, Amar MJ, et al. Cholesteryl ester transfer protein corrects dysfunctional high density lipoproteins and reduces aortic atherosclerosis in lecithin cholesterol acyltransferase transgenic mice. J Biol Chem. 1999;274(52):36912–20.PubMedCrossRef
14.
Zurück zum Zitat Furbee Jr JW, Parks JS. Transgenic overexpression of human lecithin: cholesterol acyltransferase (LCAT) in mice does not increase aortic cholesterol deposition. Atherosclerosis. 2002;165(1):89–100.PubMedCrossRef Furbee Jr JW, Parks JS. Transgenic overexpression of human lecithin: cholesterol acyltransferase (LCAT) in mice does not increase aortic cholesterol deposition. Atherosclerosis. 2002;165(1):89–100.PubMedCrossRef
15.
Zurück zum Zitat Hoeg JM, Vaisman BL, Demosky Jr SJ, et al. Lecithin:cholesterol acyltransferase overexpression generates hyperalpha-lipoproteinemia and a nonatherogenic lipoprotein pattern in transgenic rabbits. J Biol Chem. 1996;271(8):4396–402.PubMedCrossRef Hoeg JM, Vaisman BL, Demosky Jr SJ, et al. Lecithin:cholesterol acyltransferase overexpression generates hyperalpha-lipoproteinemia and a nonatherogenic lipoprotein pattern in transgenic rabbits. J Biol Chem. 1996;271(8):4396–402.PubMedCrossRef
16.
Zurück zum Zitat Brousseau ME, Hoeg JM. Transgenic rabbits as models for atherosclerosis research. J Lipid Res. 1999;40(3):365–75.PubMed Brousseau ME, Hoeg JM. Transgenic rabbits as models for atherosclerosis research. J Lipid Res. 1999;40(3):365–75.PubMed
17.
Zurück zum Zitat Brousseau ME, Santamarina-Fojo S, Vaisman BL, et al. Overexpression of human lecithin:cholesterol acyltransferase in cholesterol-fed rabbits: LDL metabolism and HDL metabolism are affected in a gene dose-dependent manner. J Lipid Res. 1997;38(12):2537–47.PubMed Brousseau ME, Santamarina-Fojo S, Vaisman BL, et al. Overexpression of human lecithin:cholesterol acyltransferase in cholesterol-fed rabbits: LDL metabolism and HDL metabolism are affected in a gene dose-dependent manner. J Lipid Res. 1997;38(12):2537–47.PubMed
18.
Zurück zum Zitat Sakai N, Vaisman BL, Koch CA, et al. Targeted disruption of the mouse lecithin:cholesterol acyltransferase (LCAT) gene. Generation of a new animal model for human LCAT deficiency. J Biol Chem. 1997;272(11):7506–10.PubMedCrossRef Sakai N, Vaisman BL, Koch CA, et al. Targeted disruption of the mouse lecithin:cholesterol acyltransferase (LCAT) gene. Generation of a new animal model for human LCAT deficiency. J Biol Chem. 1997;272(11):7506–10.PubMedCrossRef
19.
Zurück zum Zitat Lambert G, Sakai N, Vaisman BL, et al. Analysis of glomerulosclerosis and atherosclerosis in lecithin cholesterol acyltransferase-deficient mice. J Biol Chem. 2001;276(18):15090–8.PubMedCrossRef Lambert G, Sakai N, Vaisman BL, et al. Analysis of glomerulosclerosis and atherosclerosis in lecithin cholesterol acyltransferase-deficient mice. J Biol Chem. 2001;276(18):15090–8.PubMedCrossRef
20.
Zurück zum Zitat Ng DS, Maguire GF, Wylie J, et al. Oxidative stress is markedly elevated in lecithin:cholesterol acyltransferase-deficient mice and is paradoxically reversed in the apolipoprotein E knockout background in association with a reduction in atherosclerosis. J Biol Chem. 2002;277(14):11715–20.PubMedCrossRef Ng DS, Maguire GF, Wylie J, et al. Oxidative stress is markedly elevated in lecithin:cholesterol acyltransferase-deficient mice and is paradoxically reversed in the apolipoprotein E knockout background in association with a reduction in atherosclerosis. J Biol Chem. 2002;277(14):11715–20.PubMedCrossRef
21.
Zurück zum Zitat Furbee Jr JW, Sawyer JK, Parks JS. Lecithin: cholesterol acyltransferase deficiency increases atherosclerosis in the low density lipoprotein receptor and apolipoprotein E knockout mice. J Biol Chem. 2002;277(5):3511–9.PubMedCrossRef Furbee Jr JW, Sawyer JK, Parks JS. Lecithin: cholesterol acyltransferase deficiency increases atherosclerosis in the low density lipoprotein receptor and apolipoprotein E knockout mice. J Biol Chem. 2002;277(5):3511–9.PubMedCrossRef
22.
Zurück zum Zitat Amar MJ, Shamburek RD, Vaisman B, et al. Adenoviral expression of human lecithin-cholesterol acyltransferase in nonhuman primates leads to an antiatherogenic lipoprotein phenotype by increasing high-density lipoprotein and lowering low-density lipoprotein. Metabolism. 2009;58(4):568–75.PubMedCrossRef Amar MJ, Shamburek RD, Vaisman B, et al. Adenoviral expression of human lecithin-cholesterol acyltransferase in nonhuman primates leads to an antiatherogenic lipoprotein phenotype by increasing high-density lipoprotein and lowering low-density lipoprotein. Metabolism. 2009;58(4):568–75.PubMedCrossRef
23.
Zurück zum Zitat Zhou M, Sawyer J, Kelley K, et al: Abstract 5920: Lecithin Cholesterol Acyltransferase Promotes Reverse Cholesterol Transport and Attenuates Atherosclerosis Progression in New Zealand White Rabbits. Circulation 2009, 120(18_MeetingAbstracts):S1175-b-. Zhou M, Sawyer J, Kelley K, et al: Abstract 5920: Lecithin Cholesterol Acyltransferase Promotes Reverse Cholesterol Transport and Attenuates Atherosclerosis Progression in New Zealand White Rabbits. Circulation 2009, 120(18_MeetingAbstracts):S1175-b-.
24.
Zurück zum Zitat Amar MJ, D'Souza W, Turner S, et al. 5A apolipoprotein mimetic peptide promotes cholesterol efflux and reduces atherosclerosis in mice. J Pharmacol Exp Ther. 2010;334(2):634–41.PubMedCrossRef Amar MJ, D'Souza W, Turner S, et al. 5A apolipoprotein mimetic peptide promotes cholesterol efflux and reduces atherosclerosis in mice. J Pharmacol Exp Ther. 2010;334(2):634–41.PubMedCrossRef
25.
Zurück zum Zitat Tanigawa H, Billheimer JT, Tohyama J, et al. Lecithin: cholesterol acyltransferase expression has minimal effects on macrophage reverse cholesterol transport in vivo. Circulation. 2009;120(2):160–9.PubMedCrossRef Tanigawa H, Billheimer JT, Tohyama J, et al. Lecithin: cholesterol acyltransferase expression has minimal effects on macrophage reverse cholesterol transport in vivo. Circulation. 2009;120(2):160–9.PubMedCrossRef
26.
Zurück zum Zitat Wang X, Collins HL, Ranalletta M, et al. Macrophage ABCA1 and ABCG1, but not SR-BI, promote macrophage reverse cholesterol transport in vivo. J Clin Invest. 2007;117(8):2216–24.PubMedCrossRef Wang X, Collins HL, Ranalletta M, et al. Macrophage ABCA1 and ABCG1, but not SR-BI, promote macrophage reverse cholesterol transport in vivo. J Clin Invest. 2007;117(8):2216–24.PubMedCrossRef
27.
Zurück zum Zitat •• Sethi AA, Sampson M, Warnick R, et al. High pre-beta1 HDL concentrations and low lecithin: cholesterol acyltransferase activities are strong positive risk markers for ischemic heart disease and independent of HDL-cholesterol. Clin Chem. 2010;56(7):1128–37. This work demonstrates that LCAT and pre-β are good biomarkers for cardiovascular disease. PubMedCrossRef •• Sethi AA, Sampson M, Warnick R, et al. High pre-beta1 HDL concentrations and low lecithin: cholesterol acyltransferase activities are strong positive risk markers for ischemic heart disease and independent of HDL-cholesterol. Clin Chem. 2010;56(7):1128–37. This work demonstrates that LCAT and pre-β are good biomarkers for cardiovascular disease. PubMedCrossRef
28.
Zurück zum Zitat Frohlich J, Dobiasova M. Fractional esterification rate of cholesterol and ratio of triglycerides to HDL-cholesterol are powerful predictors of positive findings on coronary angiography. Clin Chem. 2003;49(11):1873–80.PubMedCrossRef Frohlich J, Dobiasova M. Fractional esterification rate of cholesterol and ratio of triglycerides to HDL-cholesterol are powerful predictors of positive findings on coronary angiography. Clin Chem. 2003;49(11):1873–80.PubMedCrossRef
29.
Zurück zum Zitat Dullaart RP, Perton F, Sluiter WJ, de Vries R, van Tol A. Plasma lecithin: cholesterol acyltransferase activity is elevated in metabolic syndrome and is an independent marker of increased carotid artery intima media thickness. J Clin Endocrinol Metab. 2008;93(12):4860–6.PubMedCrossRef Dullaart RP, Perton F, Sluiter WJ, de Vries R, van Tol A. Plasma lecithin: cholesterol acyltransferase activity is elevated in metabolic syndrome and is an independent marker of increased carotid artery intima media thickness. J Clin Endocrinol Metab. 2008;93(12):4860–6.PubMedCrossRef
30.
Zurück zum Zitat Dullaart RP, Perton F, Kappelle PJ, de Vries R, Sluiter WJ, van Tol A. Plasma lecithin: cholesterol acyltransferase activity modifies the inverse relationship of C-reactive protein with HDL cholesterol in nondiabetic men. Biochim Biophys Acta. 2010;1801(1):84–8.PubMed Dullaart RP, Perton F, Kappelle PJ, de Vries R, Sluiter WJ, van Tol A. Plasma lecithin: cholesterol acyltransferase activity modifies the inverse relationship of C-reactive protein with HDL cholesterol in nondiabetic men. Biochim Biophys Acta. 2010;1801(1):84–8.PubMed
31.
Zurück zum Zitat Hovingh GK, Hutten BA, Holleboom AG, et al. Compromised LCAT function is associated with increased atherosclerosis. Circulation. 2005;112(6):879–84.PubMedCrossRef Hovingh GK, Hutten BA, Holleboom AG, et al. Compromised LCAT function is associated with increased atherosclerosis. Circulation. 2005;112(6):879–84.PubMedCrossRef
32.
Zurück zum Zitat Holleboom AG, Duivenvoorden R, van den Bogaard B, et al: Carriers of Lcat Gene Mutations Have Increased Atherosclerosis: A 3.0 Tesla Mri Study. Atherosclerosis Supp 2010, 11(2):61-61. Holleboom AG, Duivenvoorden R, van den Bogaard B, et al: Carriers of Lcat Gene Mutations Have Increased Atherosclerosis: A 3.0 Tesla Mri Study. Atherosclerosis Supp 2010, 11(2):61-61.
33.
Zurück zum Zitat Ayyobi AF, McGladdery SH, Chan S, John Mancini GB, Hill JS, Frohlich JJ. Lecithin: cholesterol acyltransferase (LCAT) deficiency and risk of vascular disease: 25 year follow-up. Atherosclerosis. 2004;177(2):361–6.PubMedCrossRef Ayyobi AF, McGladdery SH, Chan S, John Mancini GB, Hill JS, Frohlich JJ. Lecithin: cholesterol acyltransferase (LCAT) deficiency and risk of vascular disease: 25 year follow-up. Atherosclerosis. 2004;177(2):361–6.PubMedCrossRef
34.
Zurück zum Zitat Calabresi L, Baldassarre D, Castelnuovo S, et al. Functional lecithin: cholesterol acyltransferase is not required for efficient atheroprotection in humans. Circulation. 2009;120(7):628–35.PubMedCrossRef Calabresi L, Baldassarre D, Castelnuovo S, et al. Functional lecithin: cholesterol acyltransferase is not required for efficient atheroprotection in humans. Circulation. 2009;120(7):628–35.PubMedCrossRef
35.
Zurück zum Zitat Wells IC, Peitzmeier G, Vincent JK. Lecithin: cholesterol acyltransferase and lysolecithin in coronary atherosclerosis. Exp Mol Pathol. 1986;45(3):303–10.PubMedCrossRef Wells IC, Peitzmeier G, Vincent JK. Lecithin: cholesterol acyltransferase and lysolecithin in coronary atherosclerosis. Exp Mol Pathol. 1986;45(3):303–10.PubMedCrossRef
36.
Zurück zum Zitat • Rousset X, Vaisman B, Auerbach B, et al: Effect of Recombinant Human Lecithin-cholesterol:acyltransferase Infusion on Lipoprotein Metabolism in Mice. J Pharmacol Exp Ther 2010. This work demonstates the feasibility of LCAT replacement therapy in the case of LCAT deficiency. • Rousset X, Vaisman B, Auerbach B, et al: Effect of Recombinant Human Lecithin-cholesterol:acyltransferase Infusion on Lipoprotein Metabolism in Mice. J Pharmacol Exp Ther 2010. This work demonstates the feasibility of LCAT replacement therapy in the case of LCAT deficiency.
37.
38.
Zurück zum Zitat Norum KR, Gjone E. The effect of plasma transfusion on the plasma cholesterol esters in patients with familial plasma lecithin: cholesterol acyltransferase deficiency. Scand J Clin Lab Invest. 1968;22(4):339–42.PubMedCrossRef Norum KR, Gjone E. The effect of plasma transfusion on the plasma cholesterol esters in patients with familial plasma lecithin: cholesterol acyltransferase deficiency. Scand J Clin Lab Invest. 1968;22(4):339–42.PubMedCrossRef
39.
Zurück zum Zitat Murayama N, Asano Y, Kato K, et al. Effects of plasma infusion on plasma lipids, apoproteins and plasma enzyme activities in familial lecithin: cholesterol acyltransferase deficiency. Eur J Clin Invest. 1984;14(2):122–9.PubMedCrossRef Murayama N, Asano Y, Kato K, et al. Effects of plasma infusion on plasma lipids, apoproteins and plasma enzyme activities in familial lecithin: cholesterol acyltransferase deficiency. Eur J Clin Invest. 1984;14(2):122–9.PubMedCrossRef
40.
Zurück zum Zitat Klein HG, Santamarina-Fojo S, Duverger N, et al. Fish eye syndrome: a molecular defect in the lecithin-cholesterol acyltransferase (LCAT) gene associated with normal alpha-LCAT-specific activity. Implications for classification and prognosis. The Journal of Clinical Investigation. 1993;92(1):479–85.PubMedCrossRef Klein HG, Santamarina-Fojo S, Duverger N, et al. Fish eye syndrome: a molecular defect in the lecithin-cholesterol acyltransferase (LCAT) gene associated with normal alpha-LCAT-specific activity. Implications for classification and prognosis. The Journal of Clinical Investigation. 1993;92(1):479–85.PubMedCrossRef
41.
Zurück zum Zitat Asada S, Kuroda M, Aoyagi Y, et al: Disturbed apolipoprotein A-I-containing lipoproteins in fish-eye disease are improved by the lecithin:cholesterol acyltransferase produced by gene-transduced adipocytes in vitro. Molecular Genetics and Metabolism, In Press. Asada S, Kuroda M, Aoyagi Y, et al: Disturbed apolipoprotein A-I-containing lipoproteins in fish-eye disease are improved by the lecithin:cholesterol acyltransferase produced by gene-transduced adipocytes in vitro. Molecular Genetics and Metabolism, In Press.
42.
Zurück zum Zitat • Kuroda M, Aoyagi Y, Asada S, et al: Ceiling culture-derived proliferative adipocytes are a possible delivery vehicle for enzyme replacement therapy in lecithin:cholesterol acyltransferase deficiency. Gene Ther Mol Biol. In press. This article presents an alternative to LCAT injections for a treatment of the human LCAT deficiency. • Kuroda M, Aoyagi Y, Asada S, et al: Ceiling culture-derived proliferative adipocytes are a possible delivery vehicle for enzyme replacement therapy in lecithin:cholesterol acyltransferase deficiency. Gene Ther Mol Biol. In press. This article presents an alternative to LCAT injections for a treatment of the human LCAT deficiency.
43.
Zurück zum Zitat Remaley AT, Amar M, Sviridov D. HDL-replacement therapy: mechanism of action, types of agents and potential clinical indications. Expert Rev Cardiovasc Ther. 2008;6(9):1203–15.PubMedCrossRef Remaley AT, Amar M, Sviridov D. HDL-replacement therapy: mechanism of action, types of agents and potential clinical indications. Expert Rev Cardiovasc Ther. 2008;6(9):1203–15.PubMedCrossRef
44.
Zurück zum Zitat Sethi AA, Amar M, Shamburek RD, Remaley AT. Apolipoprotein AI mimetic peptides: possible new agents for the treatment of atherosclerosis. Curr Opin Investig Drugs. 2007;8(3):201–12.PubMed Sethi AA, Amar M, Shamburek RD, Remaley AT. Apolipoprotein AI mimetic peptides: possible new agents for the treatment of atherosclerosis. Curr Opin Investig Drugs. 2007;8(3):201–12.PubMed
45.
Zurück zum Zitat • Yvan-Charvet L, Pagler T, Gautier EL, et al. ATP-binding cassette transporters and HDL suppress hematopoietic stem cell proliferation. Science. 2010;328(5986):1689–93. This article presents new data on the interaction of HDL metabolism and blood cells. PubMedCrossRef • Yvan-Charvet L, Pagler T, Gautier EL, et al. ATP-binding cassette transporters and HDL suppress hematopoietic stem cell proliferation. Science. 2010;328(5986):1689–93. This article presents new data on the interaction of HDL metabolism and blood cells. PubMedCrossRef
46.
Zurück zum Zitat Tardif JC, Heinonen T, Noble S. High-density lipoprotein/apolipoprotein A-I infusion therapy. Curr Atheroscler Rep. 2009;11(1):58–63.PubMedCrossRef Tardif JC, Heinonen T, Noble S. High-density lipoprotein/apolipoprotein A-I infusion therapy. Curr Atheroscler Rep. 2009;11(1):58–63.PubMedCrossRef
47.
Zurück zum Zitat Feister HA, Auerbach BJ, Cole LA, Krause BR, Karathanasis SK. Identification of an IL-6 response element in the human LCAT promoter. Journal of Lipid Research. 2002;43(6):960–70.PubMed Feister HA, Auerbach BJ, Cole LA, Krause BR, Karathanasis SK. Identification of an IL-6 response element in the human LCAT promoter. Journal of Lipid Research. 2002;43(6):960–70.PubMed
48.
Zurück zum Zitat Zhou M, Fordstrom P, Zhang J, et al. Novel small molecule LCAT activators raise HDL levels in rodent models. Arterioscl Throm Vas. 2008;28(6):E65–6. Zhou M, Fordstrom P, Zhang J, et al. Novel small molecule LCAT activators raise HDL levels in rodent models. Arterioscl Throm Vas. 2008;28(6):E65–6.
49.
Zurück zum Zitat Vaisman BL, Klein HG, Rouis M, et al. Overexpression of human lecithin cholesterol acyltransferase leads to hyperalphalipoproteinemia in transgenic mice. J Biol Chem. 1995;270(20):12269–75.PubMedCrossRef Vaisman BL, Klein HG, Rouis M, et al. Overexpression of human lecithin cholesterol acyltransferase leads to hyperalphalipoproteinemia in transgenic mice. J Biol Chem. 1995;270(20):12269–75.PubMedCrossRef
50.
Zurück zum Zitat Mehlum A, Staels B, Duverger N, et al. Tissue-specific expression of the human gene for lecithin: cholesterol acyltransferase in transgenic mice alters blood lipids, lipoproteins and lipases towards a less atherogenic profile. Eur J Biochem. 1995;230(2):567–75.PubMedCrossRef Mehlum A, Staels B, Duverger N, et al. Tissue-specific expression of the human gene for lecithin: cholesterol acyltransferase in transgenic mice alters blood lipids, lipoproteins and lipases towards a less atherogenic profile. Eur J Biochem. 1995;230(2):567–75.PubMedCrossRef
51.
Zurück zum Zitat Van Craeyveld E, Lievens J, Jacobs F, Feng Y, Snoeys J, De Geest B. Apolipoprotein A-I and lecithin: cholesterol acyltransferase transfer induce cholesterol unloading in complex atherosclerotic lesions. Gene Ther. 2009;16(6):757–65.PubMedCrossRef Van Craeyveld E, Lievens J, Jacobs F, Feng Y, Snoeys J, De Geest B. Apolipoprotein A-I and lecithin: cholesterol acyltransferase transfer induce cholesterol unloading in complex atherosclerotic lesions. Gene Ther. 2009;16(6):757–65.PubMedCrossRef
Metadaten
Titel
Lecithin Cholesterol Acyltransferase: An Anti- or Pro-atherogenic Factor?
verfasst von
Xavier Rousset
Robert Shamburek
Boris Vaisman
Marcelo Amar
Alan T. Remaley
Publikationsdatum
01.06.2011
Verlag
Current Science Inc.
Erschienen in
Current Atherosclerosis Reports / Ausgabe 3/2011
Print ISSN: 1523-3804
Elektronische ISSN: 1534-6242
DOI
https://doi.org/10.1007/s11883-011-0171-6

Weitere Artikel der Ausgabe 3/2011

Current Atherosclerosis Reports 3/2011 Zur Ausgabe

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Notfall-TEP der Hüfte ist auch bei 90-Jährigen machbar

26.04.2024 Hüft-TEP Nachrichten

Ob bei einer Notfalloperation nach Schenkelhalsfraktur eine Hemiarthroplastik oder eine totale Endoprothese (TEP) eingebaut wird, sollte nicht allein vom Alter der Patientinnen und Patienten abhängen. Auch über 90-Jährige können von der TEP profitieren.

Niedriger diastolischer Blutdruck erhöht Risiko für schwere kardiovaskuläre Komplikationen

25.04.2024 Hypotonie Nachrichten

Wenn unter einer medikamentösen Hochdrucktherapie der diastolische Blutdruck in den Keller geht, steigt das Risiko für schwere kardiovaskuläre Ereignisse: Darauf deutet eine Sekundäranalyse der SPRINT-Studie hin.

Bei schweren Reaktionen auf Insektenstiche empfiehlt sich eine spezifische Immuntherapie

Insektenstiche sind bei Erwachsenen die häufigsten Auslöser einer Anaphylaxie. Einen wirksamen Schutz vor schweren anaphylaktischen Reaktionen bietet die allergenspezifische Immuntherapie. Jedoch kommt sie noch viel zu selten zum Einsatz.

Therapiestart mit Blutdrucksenkern erhöht Frakturrisiko

25.04.2024 Hypertonie Nachrichten

Beginnen ältere Männer im Pflegeheim eine Antihypertensiva-Therapie, dann ist die Frakturrate in den folgenden 30 Tagen mehr als verdoppelt. Besonders häufig stürzen Demenzkranke und Männer, die erstmals Blutdrucksenker nehmen. Dafür spricht eine Analyse unter US-Veteranen.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.