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Miscellaneous

Update on the role of acyl-CoA:cholesterol acyltransferase inhibitors in atherosclerosis

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Pages 1655-1662 | Published online: 25 Feb 2005

Bibliography

  • ROSS R: The pathogenesis of atherosclerosis: an update. N Engl. j. Med. (1986) 314:488.
  • BROWN MS, HO HL, GOLDSTEIN JL: The cholesteryl ester cycle in macrophage foam cells. j. Biol. Chem. (1980) 255:9344–9352.
  • GUYTON JR, KLEMP KF: Developmentof the lipid-rich core in human atherosclerosis. Arterioscler. Thromb. Vase. Biol. (1996) 16:4–11.
  • CASES S, NOVAK S, ZHENG Y-W: ACAT-2, a second mammalian acyl-CoA:cholesterol acyltransferase. I Biol. Chem. (1998) 273:26755–26764.
  • BUHMAN KF, ACCAD M, FARESE RV JR.: Mammalian acyl-CoA:cholesterol acyltransferases. Biochim. Biophys. Acta. (2000) 1529:142–154.
  • ••This review article highlights recent studies of the molecular expression of ACAT1 and ACAT2.
  • CHANG TY, CHANG CCY, CHENG D: Acyl-CoenzymeA:cholesterol acyltransferase. Ann. Rev Biochem. (1997) 66:613–638.
  • WANG H, GERMAIN SJ, BENFIELD PB et al.: Gene expression of acyl coenzyme A: cholesterol acyltransferase is upregulated in human monocytes during differentiation and foam cell formation. Arterioscler. Thromb. Vase. Biol. (1996) 16:809–814.
  • MIYAZAKI A, SAKASHITA N, LEE 0 et al.: Expression of ACAT-1 protein in human atherosclerotic lesions and cultured human monocytes-macrophages. Arterioscler. Thromb. Vase. Biol. (1998) 18:1568–1574.
  • CHANG CYC, SAKASHITA N, ORNVOLD K et al.: Immunological quantitation and localization of ACAT-1 and ACAT-2 in human liver and small intestine. j. Biol. Chem. (2000) 275:28083–28092.
  • ••This article focuses on expression of ACATenzymes in human tissues, and concludes that there appear to be species differences, particularly with ACAT2. These findings suggest that targeting ACAT2 for inhibition in humans might not be helpful.
  • LEE RG, WILLINGHAM MC, DAVIS MA et al.: Differential expression of ACATi and ACAT2 among cells within liver, intestine, kidney, and adrenal of nonhuman primates. Lipid Res. (2000) 41:1991–2001.
  • RODRIGUEZ A, BACHORIK PS, WEE S-B: Novel effects of the acyl-Coenzyme A:cholesterol acyltransferase inhibitor 58-035 on foam cell development in primary human monocyte-derived macrophages. Arterioscler. Thromb. Vase. Biol. (1999) 19:2199–2206.
  • •This article examines novel effects of the non-specific ACAT inhibitor, 58–035, on foam cell formation in human macrophages. The results suggested that the inhibitor did not induce cytotoxicity, a finding that contrasted with increased cytotoxicity of ACAT inhibition in cultured murine macrophages.
  • RODRIGUEZ A, USHER D: Anti-atherogenic effects of the acyl-CoA:cholesterol acyltransferase, Avasimibe (CI-1011), in cultured primary human macrophages. Atherosclerosis (2001) In Press.
  • MEINER VL, CASES S, MYERS HM et al.: Disruption of the acyl-CoA:cholesterol acyltransferase gene in mice: Evidence suggesting multiple cholesterol esterification enzymes in mammals. Proc. Natl. Acad. Li. USA (1996) 93:14041–14046.
  • MATSUDA K: ACAT inhibitors as antiatherosclerotic agents: compounds and mechanisms. Med. Res. Rev (1994) 14:271–305.
  • •A comprehensive review of the structurally different compounds that are ACAT inhibitors.
  • SORBERA LA, RABASSEDA X, CASTANER J: Avasimibe, treatment of lipoprotein disorders. Drugs Fut. (1999) 24:9–15.
  • DELSING DJM, OFFERMAN EH, VAN DER ROOM H et al.: The acyl-CoA:cholesterol acyltransferase (ACAT)-inhibitor avasimibe reduces atherosclerosis independently of its lipid-lowering effect in cholesterol-fed apoE3-Leiden transgenic mice. Circulation (Suppl.) (1999) Abstract 3232.
  • BOCAN TMA, KRAUSE BR, ROSEBURY WS etal.: The ACAT inhibitor avasimibe reduces macrophages and matrix metalloproteinase expression in atherosclerotic lesions of hypercholesterolemic rabbits. Arterioscler. Thromb. Vase. Biol. (2000) 20:70–79.
  • CULLEN P, CIGNARELLA A, ASSMANN G: The effects of atorvastatin, the ACAT inhibitor CI-1011, and progesterone on storage and secretion of cholesterol in human monocyte-derived macrophages. Circulation (1998) Abstract 2828.
  • INSULL W, KOREN M, DAVIGNON J et al.: Efficacy and short-term safety of a new ACAT inhibitor, avasimibe, on lipids, lipoproteins, and apolipoproteins, in patients with combined hyperlipidemia. Atherosclerosis (2001) In PITS&
  • •A recent publication examining the effects of CI-1011 in patients. The results showed a significant decrease in triglyceride levels, but no apparent increase in side effects.
  • WU J, DOSHI R, RODRIGUEZ A: An update of acyl-CoA:cholesterol acyltransferase inhibition in animal and human in vitro and in vivo models of atherosclerosis. Curr. Med. Chein.-Inon. Eridoc. & Metall. Agents (2001) 1:141–150.
  • RUDEL LL, LEE RG, COCKMAN TL: Acyl coenzyme A: cholesterol acyltransferase types 1 and 2: structure and function in atherosclerosis. Curr. Opiri. Lipidol. (2001) 12:121–127.
  • BUHMAN KF, ACCAD M, FARESE RV JR: Mammalian acyl-CoA:cholesterol acyltransferases. Biochlin. Biophys. Acta. (2000) 1529:142–154.
  • JOYCE C, STUNNER K, ANDERSON RA et al.: Acyl-coenzyme A:cholesterol acyltransferase 2. Curr. Opin. Lipidol. (1999) 10:89–95.
  • NICOLOSI RJ, WILSON TA, KRAUSE BR: The ACAT inhibitor, CI-1011 is effective in the prevention and regression of aortic fatty streak in hamsters. Atherosclerosis (1998) 137:77–85.
  • WILCOX LJ, BARRETT PHR, NEWTON RS et al.: ApoB100 secretion from HepG2 cells is decreased by the ACAT inhibitor CI-1011. Arterioscler. Thromb. Vasc. Biol. (1999) 19:939–949.
  • SHIN YW, BOK S-H, JEONG T-S etal.:Hypocholesterolemic effect of naringin associated with hepatic cholesterol regulating enzyme changes in rats. Int. Nutr. Res. (1999) 69:341–347.
  • LEE SH, PARK YB, BAE KH et al.: Cholesterol-lowering activity of naringenin via inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase and acyl coenzyme-A:cholesterol acyltransferase in rats. Ann. Nutr. Metab. (1999) 43:173–180.
  • BOK S-H, LEE S-H, PARK Y-B etal.: Plasma and hepatic cholesterol and hepatic activities of 3-hydroxy-3-methyl-glutaryl-CoA reductase and acyl CoA:cholesterol transferase are lower in rats fed citrus peel extract or a mixture of citrus bioflavonoids. J.Nutr (1999) 129:1182–1185.
  • NISHIMURA K, FUKUDA T, MIYASE T etal.: Activity-guided isolation of triterpenoid acyl-CoA:cholesterol acyltransferase (ACAT) inhibitors from Ilex kudiricha. J. Nat. Prod. (1999) 62:1061–1064.
  • NISHIMURA K, MIYASE T, NOGUCHI H: Triterpenoid saponins from Ilex kudiricha. j Nat. Prod. (1999) 62:1128–1133.
  • FAZIO S, MAJOR SS, SWIFT LL etal.:Increased atherosclerosis in LDL receptor-null mice lacking ACATi in macrophages. Chi]. Invest. (2001) 107:163–171.
  • ACCAD M, SMITH SJ, NEWLAND DL etal.: Massive xanthomatosis and altered composition of atherosclerotic lesions in hyperlipidemic mice lacking acyl CoA:cholesterol acyltransferase 1. _J. Clin Invest. (2000) 105:711–719.
  • KUSUNOKI J, HANSOTY DK, ARAGANE K et al.: Acyl-CoA:cholesterol acyltransferase inhibition reduces atherosclerosis in apolipoprotein E-deficient mice. Circulation (2001) 103:2604–2609.
  • HARRIS WS, DUJOVNE CA, VON BERGMANN K et al.: Effects of the ACAT inhibitor CL 277, 082 on cholesterol metabolism in humans. Chi]. Pharincol. Ther. (1990) 48:189–194.
  • HAINER JW, TERRY JG, CONNELL JM etal.: Effect of the acyl-CoA:cholesterol acyltransferase inhibitor DUP128 on cholesterol absorption and serum cholesterol in humans. Chi]. Phannacol. Ther. (1994) 56:65–74.
  • PECK RW, WIGGS R, POSNER J: The tolerability, pharmacokinetics and lack of effect on plasma cholesterol of 447C88, an acyl-CoA:cholesterol acyltransferase (ACAT) inhibitor with low bioavailability, in healthy volunteers. Eur. j CBI]. Pharmacol. (1995) 49:243–249.

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