摘要
背景：血脂异常是动脉粥样硬化的公认危险因素，然而，通过研究增强HDL胆固醇的疗法的试验揭示的新证据表明，当HDL-C高时，动脉粥样硬化风险增加。 结果：一些研究强调了功能失调的脂蛋白在动脉粥样硬化疾病中的核心作用; 根据动脉粥样硬化病变的“氧化假说”，氧化的LDL-胆固醇是一个重要特征，然而，今天对功能失调的HDL-胆固醇的兴趣日益增加。 我们的论文的目标是回顾修饰和功能失调的脂蛋白在动脉粥样硬化形成中的功能。 结论：考虑到功能失调的脂蛋白的中心作用，脂蛋白功能特征的测量，而不是常规的脂蛋白常规血清评估，可以在实验研究中提供有效的贡献，如在临床实践中分层动脉粥样硬化风险。
关键词: 脂蛋白，氧化，功能失调，动脉粥样硬化，血脂异常，高密度脂蛋白胆固醇，动脉粥样硬化。
[1]
Kontush, A.; Chapman, M.J. Antiatherogenic small, dense HDL--guardian angel of the arterial wall? Nat. Clin. Pract. Cardiovasc. Med., 2006, 3(3), 144-153.
[2]
Barter, P.; Kastelein, J.; Nunn, A.; Hobbs, R. High density lipoproteins (HDLs) and atherosclerosis; the unanswered questions. Atherosclerosis, 2003, 168(2), 195-211.
[3]
Maron, D.J.; Fazio, S.; Linton, M.F. Current perspectives on statins. Circulation, 2000, 101(2), 207-213.
[4]
Barquera, S.; Pedroza-Tobías, A.; Medina, C.; Hernández-Barrera, L.; Bibbins-Domingo, K.; Lozano, R.; Moran, A.E. Global overview of the epidemiology of atherosclerotic cardiovascular disease. Arch. Med. Res., 2015, 46(5), 328-338.
[5]
Di Raimondo, D.; Miceli, G.; Musiari, G.; Tuttolomondo, A.; Pinto, A. New insights about the putative role of myokines in the context of cardiac rehabilitation and secondary cardiovascular prevention. Ann. Transl. Med., 2017, 5(15), 300.
[6]
Di Raimondo, D.; Musiari, G.; Miceli, G.; Arnao, V.; Pinto, A. Preventive and therapeutic role of muscle contraction against chronic diseases. Curr. Pharm. Des., 2016, 22(30), 4686-4699.
[7]
Di Raimondo, D.; Tuttolomondo, A.; Musiari, G.; Schimmenti, C.; D’Angelo, A.; Pinto, A. Are the myokines the mediators of physical activity-induced health benefits? Curr. Pharm. Des., 2016, 22(24), 3622-3647.
[8]
Di Raimondo, D.; Tuttolomondo, A.; Buttà, C.; Casuccio, A.; Giarrusso, L.; Miceli, G.; Licata, G.; Pinto, A. Metabolic and anti-inflammatory effects of a home-based programme of aerobic physical exercise. Int. J. Clin. Pract., 2013, 67(12), 1247-1253.
[9]
Anderson, K.M.; Castelli, W.P.; Levy, D. Cholesterol and mortality. 30 years of follow-up from the Framingham study. JAMA, 1987, 257(16), 2176-2180.
[10]
Martin, M.J.; Hulley, S.B.; Browner, W.S.; Kuller, L.H.; Wentworth, D. Serum cholesterol, blood pressure, and mortality: implications from a cohort of 361,662 men. Lancet, 1986, 2(8513), 933-936.
[11]
Tsimikas, S.; Brilakis, E.S.; Miller, E.R.; McConnell, J.P.; Lennon, R.J.; Kornman, K.S.; Witztum, J.L.; Berger, P.B. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease. N. Engl. J. Med., 2005, 353(1), 46-57.
[12]
Roger, V.L.; Go, A.S.; Lloyd-Jones, D.M.; Benjamin, E.J.; Berry, J.D.; Borden, W.B.; Bravata, D.M.; Dai, S.; Ford, E.S.; Fox, C.S.; Fullerton, H.J.; Gillespie, C.; Hailpern, S.M.; Heit, J.A.; Howard, V.J.; Kissela, B.M.; Kittner, S.J.; Lackland, D.T.; Lichtman, J.H.; Lisabeth, L.D.; Makuc, D.M.; Marcus, G.M.; Marelli, A.; Matchar, D.B.; Moy, C.S.; Mozaffarian, D.; Mussolino, M.E.; Nichol, G.; Paynter, N.P.; Soliman, E.Z.; Sorlie, P.D.; Sotoodehnia, N.; Turan, T.N.; Virani, S.S.; Wong, N.D.; Woo, D.; Turner, M.B. American heart association statistics committee and stroke statistics subcommittee. heart disease and stroke statistics--2012 update: a report from the american heart association. Circulation, 2012, 125(1), e2-e220.
[14]
Roger, V.L.; Go, A.S.; Lloyd-Jones, D.M.; Adams, R.J.; Berry, J.D.; Brown, T.M.; Carnethon, M.R.; Dai, S.; de Simone, G.; Ford, E.S.; Fox, C.S.; Fullerton, H.J.; Gillespie, C.; Greenlund, K.J.; Hailpern, S.M.; Heit, J.A.; Ho, P.M.; Howard, V.J.; Kissela, B.M.; Kittner, S.J.; Lackland, D.T.; Lichtman, J.H.; Lisabeth, L.D.; Makuc, D.M.; Marcus, G.M.; Marelli, A.; Matchar, D.B.; McDermott, M.M.; Meigs, J.B.; Moy, C.S.; Mozaffarian, D.; Mussolino, M.E.; Nichol, G.; Paynter, N.P.; Rosamond, W.D.; Sorlie, P.D.; Stafford, R.S.; Turan, T.N.; Turner, M.B.; Wong, N.D.; Wylie-Rosett, J. American heart association statistics committee and stroke statistics subcommittee. Heart disease and stroke statistics--2011 update: a report from the American heart association. Circulation, 2011, 123(4), e18-e209.
[15]
Centers for Disease Control and Prevention (CDC). State-specific cholesterol screening trends: United States, 1991–1999. MMWR Morb. Mortal. Wkly. Rep., 2001, 50(35), 754-758.
[16]
Zhang, L.; Qiao, Q.; Tuomilehto, J.; Hammar, N.; Ruotolo, G.; Stehouwer, C.D.; Heine, R.J.; Eliasson, M.; Zethelius, B. DECODE Study Group. The impact of dyslipidaemia on cardiovascular mortality in individuals without a prior history of diabetes in the DECODE Study. Atherosclerosis, 2009, 206(1), 298-302.
[17]
Fodor, J.G.; Frohlich, J.J.; Genest, J.J.G., Jr; McPherson, P.R. Recommendations for the management and treatment of dyslipidemia. CMAJ, 2000, 162(10), 1441-1447.
[18]
Stancu, C.S.; Toma, L.; Sima, A.V. Dual role of lipoproteins in endothelial cell dysfunction in atherosclerosis. Cell Tissue Res., 2012, 349(2), 433-446.
[19]
Mayes, P.A. Cholesterol synthesis, transport, and excretion. Harper’s Biochem 23., 1993, 266-278.
[20]
Johansson, J.; Carlson, L.A.; Landou, C.; Hamsten, A. High density lipoproteins and coronary atherosclerosis. A strong inverse relation with the largest particles is confined to normotriglyceridemic patients. Arterioscler. Thromb., 1991, 11(1), 174-182.
[21]
Rosenson, R.S.; Brewer, H.B., Jr; Chapman, M.J.; Fazio, S.; Hussain, M.M.; Kontush, A.; Krauss, R.M.; Otvos, J.D.; Remaley, A.T.; Schaefer, E.J. HDL measures, particle heterogeneity, proposed nomenclature, and relation to atherosclerotic cardiovascular events. Clin. Chem., 2011, 57(3), 392-410.
[22]
El Harchaoui, K.; Arsenault, B.J.; Franssen, R.; Després, J.P.; Hovingh, G.K.; Stroes, E.S.G.; Otvos, J.D.; Wareham, N.J.; Kastelein, J.J.; Khaw, K.T.; Boekholdt, S.M. High-density lipoprotein particle size and concentration and coronary risk. Ann. Intern. Med., 2009, 150(2), 84-93.
[23]
Champe, P.C.; Harvey, R.A. Cholesterol and steroid metabolism. Lippincott’s illustrated reviews. Biochem 2., 1994, 205-228.
[24]
Marinetti, G. V. Dietary management of elevated blood
lipids. Disorders of lipid metabolism., 1990, 135-168.
[25]
Attie, A.D.; Kastelein, J.P.; Hayden, M.R. Pivotal role of ABCA1 in reverse cholesterol transport influencing HDL levels and susceptibility to atherosclerosis. J. Lipid Res., 2001, 42(11), 1717-1726.
[26]
Ansell, B.J.; Fonarow, G.C.; Fogelman, A.M. The paradox of dysfunctional high-density lipoprotein. Curr. Opin. Lipidol., 2007, 18(4), 427-434.
[27]
Bermúdez, V.; Cano, R.; Cano, C.; Bermúdez, F.; Arraiz, N.; Acosta, L.; Finol, F.; Pabón, M.R.; Amell, A.; Reyna, N.; Hidalgo, J.; Kendall, P.; Manuel, V.; Hernández, R. Pharmacologic management of isolated low high-density lipoprotein syndrome. Am. J. Ther., 2008, 15(4), 377-388.
[28]
Brousseau, M.E.; Schaefer, E.J.; Wolfe, M.L.; Bloedon, L.T.; Digenio, A.G.; Clark, R.W.; Mancuso, J.P.; Rader, D.J. Effects of an inhibitor of cholesteryl ester transfer protein on HDL cholesterol. N. Engl. J. Med., 2004, 350(15), 1505-1515.
[29]
Kastelein, J.J.; van Leuven, S.I.; Burgess, L.; Evans, G.W.; Kuivenhoven, J.A.; Barter, P.J.; Revkin, J.H.; Grobbee, D.E.; Riley, W.A.; Shear, C.L.; Duggan, W.T.; Bots, M.L. RADIANCE 1 Investigators. Effect of torcetrapib on carotid atherosclerosis in familial hypercholesterolemia. N. Engl. J. Med., 2007, 356(16), 1620-1630.
[30]
Ansell, B.J.; Fonarow, G.C.; Fogelman, A.M. High-density lipoprotein: is it always atheroprotective? Curr. Atheroscler. Rep., 2006, 8(5), 405-411.
[31]
Norata, G.D.; Pirillo, A.; Catapano, A.L. Statins and oxidative stress during atherogenesis. J. Cardiovasc. Risk, 2003, 10(3), 181-189.
[32]
Leeuwenburgh, C.; Hardy, M.M.; Hazen, S.L.; Wagner, P.; Oh-ishi, S.; Steinbrecher, U.P.; Heinecke, J.W. Reactive nitrogen intermediates promote low density lipoprotein oxidation in human atherosclerotic intima. J. Biol. Chem., 1997, 272(3), 1433-1436.
[33]
Lougheed, M.; Steinbrecher, U.P. Mechanism of uptake of copper-oxidized low density lipoprotein in macrophages is dependent on its extent of oxidation. J. Biol. Chem., 1996, 271(20), 11798-11805.
[34]
Navab, M.; Imes, S.S.; Hama, S.Y.; Hough, G.P.; Ross, L.A.; Bork, R.W.; Valente, A.J.; Berliner, J.A.; Drinkwater, D.C.; Laks, H. Monocyte transmigration induced by modification of low density lipoprotein in cocultures of human aortic wall cells is due to induction of monocyte chemotactic protein 1 synthesis and is abolished by high density lipoprotein. J. Clin. Invest., 1991, 88(6), 2039-2046.
[35]
Choi, S.H.; Sviridov, D.; Miller, Y.I. Oxidized cholesteryl esters and inflammation. Biochim. Biophys. Acta Mol. Cell Biol. Lipids, 2017, 1862(4), 393-397.
[36]
Esterbauer, H.; Jürgens, G.; Quehenberger, O.; Koller, E. Autoxidation of human low density lipoprotein: loss of polyunsaturated fatty acids and vitamin E and generation of aldehydes. J. Lipid Res., 1987, 28(5), 495-509.
[37]
Parthasarathy, S.; Steinbrecher, U.P.; Barnett, J.; Witztum, J.L.; Steinberg, D. Essential role of phospholipase A2 activity in endothelial cell-induced modification of low density lipoprotein. Proc. Natl. Acad. Sci. USA, 1985, 82(9), 3000-3004.
[38]
Goldstein, J.L.; Ho, Y.K.; Basu, S.K.; Brown, M.S. Binding site on macrophages that mediates uptake and degradation of acetylated low density lipoprotein, producing massive cholesterol deposition. Proc. Natl. Acad. Sci. USA, 1979, 76(1), 333-337.
[39]
Heinecke, J.W.; Rosen, H.; Chait, A. Iron and copper promote modification of low density lipoprotein by human arterial smooth muscle cells in culture. J. Clin. Invest., 1984, 74(5), 1890-1894.
[40]
Henriksen, T.; Mahoney, E.M.; Steinberg, D. Enhanced macrophage degradation of low density lipoprotein previously incubated with cultured endothelial cells: recognition by receptors for acetylated low density lipoproteins. Proc. Natl. Acad. Sci. USA, 1981, 78(10), 6499-6503.
[41]
Parthasarathy, S.; Printz, D.J.; Boyd, D.; Joy, L.; Steinberg, D. Macrophage oxidation of low density lipoprotein generates a modified form recognized by the scavenger receptor. Arteriosclerosis, 1986, 6(5), 505-510.
[42]
Liao, J.K.; Shin, W.S.; Lee, W.Y.; Clark, S.L. Oxidized low-density lipoprotein decreases the expression of endothelial nitric oxide synthase. J. Biol. Chem., 1995, 270(1), 319-324.
[43]
Kugiyama, K.; Kerns, S.A.; Morrisett, J.D.; Roberts, R.; Henry, P.D. Impairment of endothelium-dependent arterial relaxation by lysolecithin in modified low-density lipoproteins. Nature, 1990, 344(6262), 160-162.
[44]
Witztum, J.L.; Steinberg, D. Role of oxidized low density lipoprotein in atherogenesis. J. Clin. Invest., 1991, 88(6), 1785-1792.
[45]
Murohara, T.; Kugiyama, K.; Ohgushi, M.; Sugiyama, S.; Ohta, Y.; Yasue, H. LPC in oxidized LDL elicits vasocontraction and inhibits endothelium- dependent relaxation. Am. J. Physiol., 1994, 267(6 Pt 2), H2441-H2449.
[46]
Quinn, M.T.; Parthasarathy, S.; Steinberg, D. Lysophosphatidylcholine: a chemotactic factor for human monocytes and its potential role in atherogenesis. Proc. Natl. Acad. Sci. USA, 1988, 85(8), 2805-2809.
[47]
Aviram, M. Modified forms of low density lipoprotein affect platelet aggregation in vitro. Thromb. Res., 1989, 53(6), 561-567.
[48]
Kugiyama, K.; Sakamoto, T.; Misumi, I.; Sugiyama, S.; Ohgushi, M.; Ogawa, H.; Horiguchi, M.; Yasue, H. Transferable lipids in oxidized low-density lipoprotein stimulate plasminogen activator inhibitor-1 and inhibit tissue-type plasminogen activator release from endothelial cells. Circ. Res., 1993, 73(2), 335-343.
[49]
White, D. A. The phospholipid composition in mammalian
tissues. Form and function of phospholipids, 1973, 441-
482.
[50]
Liu, S-Y.; Lu, X.; Choy, S.; Dembinski, T.C.; Hatch, G.M.; Mymin, D.; Shen, X.; Angel, A.; Choy, P.C.; Man, R.Y.K. Alteration of lysophosphatidylcholine content in low density lipoprotein after oxidative modification: relationship to endothelium dependent relaxation. Cardiovasc. Res., 1994, 28(10), 1476-1481.
[51]
Yokoyama, M.; Hirata, K.; Miyake, R.; Akita, H.; Ishikawa, Y.; Fukuzaki, H. Lysophosphatidylcholine: essential role in the inhibition of endothelium-dependent vasorelaxation by oxidized low density lipoprotein. Biochem. Biophys. Res. Commun., 1990, 168(1), 301-308.
[52]
Simon, B.C.; Cunningham, L.D.; Cohen, R.A. Oxidized low density lipoproteins cause contraction and inhibit endothelium-dependent relaxation in the pig coronary artery. J. Clin. Invest., 1990, 86(1), 75-79.
[53]
Hirata, K.; Miki, N.; Kuroda, Y.; Sakoda, T.; Kawashima, S.; Yokoyama, M. Low concentration of oxidized low-density lipoprotein and lysophosphatidylcholine upregulate constitutive nitric oxide synthase mRNA expression in bovine aortic endothelial cells. Circ. Res., 1995, 76(6), 958-962.
[54]
Choy, P.C.; Siow, Y.L.; Mymin, D. O, K. Lipids and atherosclerosis. Biochem. Cell Biol., 2004, 82(1), 212-224.
[55]
Calabresi, L.; Gomaraschi, M.; Franceschini, G. Endothelial protection by high-density lipoproteins: from bench to bedside. Arterioscler. Thromb. Vasc. Biol., 2003, 23(10), 1724-1731.
[56]
Norata, G.D.; Catapano, A.L. Molecular mechanisms responsible for the antiinflammatory and protective effect of HDL on the endothelium. Vasc. Health Risk Manag., 2005, 1(2), 119-129.
[57]
Nofer, J.R.; Kehrel, B.; Fobker, M.; Levkau, B.; Assmann, G.; von Eckardstein, A. HDL and arteriosclerosis: beyond reverse cholesterol transport. Atherosclerosis, 2002, 161(1), 1-16.
[58]
Norata, G.D.; Pirillo, A.; Catapano, A.L. Modified HDL: biological and physiopathological consequences. Nutr. Metab. Cardiovasc. Dis., 2006, 16(5), 371-386.
[59]
Navab, M.; Hama, S.Y.; Hough, G.P.; Subbanagounder, G.; Reddy, S.T.; Fogelman, A.M. A cell-free assay for detecting HDL that is dysfunctional in preventing the formation of or inactivating oxidized phospholipids. J. Lipid Res., 2001, 42(8), 1308-1317.
[60]
Bérard, A.M.; Föger, B.; Remaley, A.; Shamburek, R.; Vaisman, B.L.; Talley, G.; Paigen, B.; Hoyt, R.F., Jr; Marcovina, S.; Brewer, H.B., Jr; Santamarina-Fojo, S. High plasma HDL concentrations associated with enhanced atherosclerosis in transgenic mice overexpressing lecithin-cholesteryl acyltransferase. Nat. Med., 1997, 3(7), 744-749.
[61]
Link, J.J.; Rohatgi, A.; de Lemos, J.A. HDL cholesterol: physiology, pathophysiology, and management. Curr. Probl. Cardiol., 2007, 32(5), 268-314.
[62]
Navab, M.; Hama, S.Y.; Cooke, C.J.; Anantharamaiah, G.M.; Chaddha, M.; Jin, L.; Subbanagounder, G.; Faull, K.F.; Reddy, S.T.; Miller, N.E.; Fogelman, A.M. Normal high density lipoprotein inhibits three steps in the formation of mildly oxidized low density lipoprotein: step 1. J. Lipid Res., 2000, 41(9), 1481-1494.
[63]
Navab, M.; Ananthramaiah, G.M.; Reddy, S.T.; Van Lenten, B.J.; Ansell, B.J.; Fonarow, G.C.; Vahabzadeh, K.; Hama, S.; Hough, G.; Kamranpour, N.; Berliner, J.A.; Lusis, A.J.; Fogelman, A.M. The oxidation hypothesis of atherogenesis: the role of oxidized phospholipids and HDL. J. Lipid Res., 2004, 45(6), 993-1007.
[64]
Navab, M.; Hama, S.Y.; Anantharamaiah, G.M.; Hassan, K.; Hough, G.P.; Watson, A.D.; Reddy, S.T.; Sevanian, A.; Fonarow, G.C.; Fogelman, A.M. Normal high density lipoprotein inhibits three steps in the formation of mildly oxidized low density lipoprotein: steps 2 and 3. J. Lipid Res., 2000, 41(9), 1495-1508.
[65]
Navab, M.; Berliner, J.A.; Subbanagounder, G.; Hama, S.; Lusis, A.J.; Castellani, L.W.; Reddy, S.; Shih, D.; Shi, W.; Watson, A.D.; Van Lenten, B.J.; Vora, D.; Fogelman, A.M. HDL and the inflammatory response induced by LDL-derived oxidized phospholipids. Arterioscler. Thromb. Vasc. Biol., 2001, 21(4), 481-488.
[66]
Shih, D.M.; Xia, Y.R.; Wang, X.P.; Miller, E.; Castellani, L.W.; Subbanagounder, G.; Cheroutre, H.; Faull, K.F.; Berliner, J.A.; Witztum, J.L.; Lusis, A.J. Combined serum paraoxonase knockout/apolipoprotein E knockout mice exhibit increased lipoprotein oxidation and atherosclerosis. J. Biol. Chem., 2000, 275(23), 17527-17535.
[67]
Tward, A.; Xia, Y.R.; Wang, X.P.; Shi, Y.S.; Park, C.; Castellani, L.W.; Lusis, A.J.; Shih, D.M. Decreased atherosclerotic lesion formation in human serum paraoxonase transgenic mice. Circulation, 2002, 106(4), 484-490.
[68]
Tselepis, A.D.; John Chapman, M. Inflammation, bioactive lipids and atherosclerosis: potential roles of a lipoprotein-associated phospholipase A2, platelet activating factor-acetylhydrolase. Atheroscler. Suppl., 2002, 3(4), 57-68.
[69]
Aviram, M.; Rosenblat, M. Paraoxonases 1, 2, and 3, oxidative stress, and macrophage foam cell formation during atherosclerosis development. Free Radic. Biol. Med., 2004, 37(9), 1304-1316.
[70]
Forte, T.M.; Subbanagounder, G.; Berliner, J.A.; Blanche, P.J.; Clermont, A.O.; Jia, Z.; Oda, M.N.; Krauss, R.M.; Bielicki, J.K. Altered activities of anti-atherogenic enzymes LCAT, paraoxonase, and platelet-activating factor acetylhydrolase in atherosclerosis-susceptible mice. J. Lipid Res., 2002, 43(3), 477-485.
[71]
Negre-Salvayre, A.; Dousset, N.; Ferretti, G.; Bacchetti, T.; Curatola, G.; Salvayre, R. Antioxidant and cytoprotective properties of high-density lipoproteins in vascular cells. Free Radic. Biol. Med., 2006, 41(7), 1031-1040.
[72]
Rosenblat, M.; Vaya, J.; Shih, D.; Aviram, M. Paraoxonase 1 (PON1) enhances HDL-mediated macrophage cholesterol efflux via the ABCA1 transporter in association with increased HDL binding to the cells: a possible role for lysophosphatidylcholine. Atherosclerosis, 2005, 179(1), 69-77.
[73]
Ansell, B.J.; Fonarow, G.C.; Fogelman, A.M. The paradox of dysfunctional high-density lipoprotein. Curr. Opin. Lipidol., 2007, 18(4), 427-434.
[74]
Galle, J.; Ochslen, M.; Schollmeyer, P.; Wanner, C. Oxidized lipoproteins inhibit endothelium-dependent vasodilation. Effects of pressure and high-density lipoprotein. Hypertension, 1994, 23(5), 556-564.
[75]
Navab, M.; Hama, S.Y.; Hough, G.P.; Subbanagounder, G.; Reddy, S.T.; Fogelman, A.M. A cell-free assay for detecting HDL that is dysfunctional in preventing the formation of or inactivating oxidized phospholipids. J. Lipid Res., 2001, 42(8), 1308-1317.
[76]
Watson, A.D.; Navab, M.; Hama, S.Y.; Sevanian, A.; Prescott, S.M.; Stafforini, D.M.; McIntyre, T.M.; Du, B.N.; Fogelman, A.M.; Berliner, J.A. Effect of platelet activating factor-acetylhydrolase on the formation and action of minimally oxidized low density lipoprotein. J. Clin. Invest., 1995, 95(2), 774-782.
[77]
Mackness, M.I.; Arrol, S.; Durrington, P.N. Paraoxonase prevents accumulation of lipoperoxides in low-density lipoprotein. FEBS Lett., 1991, 286(1-2), 152-154.
[78]
Aviram, M.; Rosenblat, M.; Bisgaier, C.L.; Newton, R.S.; Primo-Parmo, S.L.; La Du, B.N. Paraoxonase inhibits high-density lipoprotein oxidation and preserves its functions. A possible peroxidative role for paraoxonase. J. Clin. Invest., 1998, 101(8), 1581-1590.
[79]
Aviram, M.; Hardak, E.; Vaya, J.; Mahmood, S.; Milo, S.; Hoffman, A.; Billicke, S.; Draganov, D.; Rosenblat, M. Human serum paraoxonases (PON1) Q and R selectively decrease lipid peroxides in human coronary and carotid atherosclerotic lesions: PON1 esterase and peroxidase-like activities. Circulation, 2000, 101(21), 2510-2517.
[80]
Shih, D.M.; Xia, Y.R.; Wang, X.P.; Miller, E.; Castellani, L.W.; Subbanagounder, G.; Cheroutre, H.; Faull, K.F.; Berliner, J.A.; Witztum, J.L.; Lusis, A.J. Combined serum paraoxonase knockout/apolipoprotein E knockout mice exhibit increased lipoprotein oxidation and atherosclerosis. J. Biol. Chem., 2000, 275(23), 17527-17535.
[81]
Stafforini, D.M.; Zimmerman, G.A.; McIntyre, T.M.; Prescott, S.M. The platelet-activating factor acetylhydrolase from human plasma prevents oxidative modification of low-density lipoprotein. Trans. Assoc. Am. Physicians, 1992, 105, 44-63.
[82]
Watson, A.D.; Berliner, J.A.; Hama, S.Y.; La Du, B.N.; Faull, K.F.; Fogelman, A.M.; Navab, M. Protective effect of high density lipoprotein associated paraoxonase. Inhibition of the biological activity of minimally oxidized low density lipoprotein. J. Clin. Invest., 1995, 96(6), 2882-2891.
[83]
Goyal, J.; Wang, K.; Liu, M.; Subbaiah, P.V. Novel function of lecithin-cholesterol acyltransferase. Hydrolysis of oxidized polar phospholipids generated during lipoprotein oxidation. J. Biol. Chem., 1997, 272(26), 16231-16239.
[84]
Liu, M.; St Clair, R.W.; Subbaiah, P.V. Impaired function of lecithin: cholesterol acyltransferase in atherosclerosis-susceptible White Carneau pigeons: possible effects on metabolism of oxidized phospholipids. J. Lipid Res., 1998, 39(2), 245-254.
[85]
Subramanian, V.S.; Goyal, J.; Miwa, M.; Sugatami, J.; Akiyama, M.; Liu, M.; Subbaiah, P.V. Role of lecithin-cholesterol acyltransferase in the metabolism of oxidized phospholipids in plasma: studies with platelet-activating factor-acetyl hydrolase-deficient plasma. Biochim. Biophys. Acta, 1999, 1439(1), 95-109.
[86]
Vohl, M.C.; Neville, T.A.; Kumarathasan, R.; Braschi, S.; Sparks, D.L. A novel lecithin-cholesterol acyltransferase antioxidant activity prevents the formation of oxidized lipids during lipoprotein oxidation. Biochem., 1999, 38(19), 5976-5981.
[87]
Itabe, H.; Hosoya, R.; Karasawa, K.; Jimi, S.; Saku, K.; Takebayashi, S.; Imanaka, T.; Takano, T. Metabolism of oxidized phosphatidylcholines formed in oxidized low density lipoprotein by lecithin-cholesterol acyltransferase. J. Biochem., 1999, 126(1), 153-161.
[88]
Chen, N.; Liu, Y.; Greiner, C.D.; Holtzman, J.L. Physiologic concentrations of homocysteine inhibit the human plasma GSH peroxidase that reduces organic hydroperoxides. J. Lab. Clin. Med., 2000, 136(1), 58-65.
[89]
Nagano, Y.; Arai, H.; Kita, T. High density lipoprotein loses its effect to stimulate efflux of cholesterol from foam cells after oxidative modification. Proc. Natl. Acad. Sci. USA, 1991, 88(15), 6457-6461.
[90]
Hurtado, I.; Fiol, C.; Gracia, V.; Caldú, P. In vitro oxidised HDL exerts a cytotoxic effect on macrophages. Atherosclerosis, 1996, 125(1), 39-46.
[91]
Nakajima, T.; Origuchi, N.; Matsunaga, T.; Kawai, S.; Hokari, S.; Nakamura, H.; Inoue, I.; Katayama, S.; Nagata, A.; Komoda, T. Localization of oxidized HDL in atheromatous plaques and oxidized HDL binding sites on human aortic endothelial cells. Ann. Clin. Biochem., 2000, 37(Pt 2), 179-186.
[92]
Matsunaga, T.; Hokari, S.; Koyama, I.; Harada, T.; Komoda, T. NF-kappa B activation in endothelial cells treated with oxidized high-density lipoprotein. Biochem. Biophys. Res. Commun., 2003, 303(1), 313-319.
[93]
Daugherty, A.; Dunn, J.L.; Rateri, D.L.; Heinecke, J.W. Myeloperoxidase, a catalyst for lipoprotein oxidation, is expressed in human atherosclerotic lesions. J. Clin. Invest., 1994, 94(1), 437-444.
[94]
Bergt, C.; Reicher, H.; Malle, E.; Sattler, W. Hypochlorite modification of high density lipoprotein: effects on cholesterol efflux from J774 macrophages. FEBS Lett., 1999, 452(3), 295-300.
[95]
Marsche, G.; Hammer, A.; Oskolkova, O.; Kozarsky, K.F.; Sattler, W.; Malle, E. Hypochlorite-modified high density lipoprotein, a high affinity ligand to scavenger receptor class B, type I, impairs high density lipoprotein-dependent selective lipid uptake and reverse cholesterol transport. J. Biol. Chem., 2002, 277(35), 32172-32179.
[96]
Suc, I.; Brunet, S.; Mitchell, G.; Rivard, G.E.; Levy, E. Oxidative tyrosylation of high density lipoproteins impairs cholesterol efflux from mouse J774 macrophages: role of scavenger receptors, classes A and B. J. Cell Sci., 2003, 116(Pt 1), 89-99.
[97]
Lee, M.; Lindstedt, L.K.; Kovanen, P.T. Mast cell-mediated inhibition of reverse cholesterol transport. Arterioscler. Thromb., 1992, 12(11), 1329-1335.
[98]
Lindstedt, L.; Saarinen, J.; Kalkkinen, N.; Welgus, H.; Kovanen, P.T. Matrix metalloproteinases-3, -7, and -12, but not -9, reduce high density lipoprotein-induced cholesterol efflux from human macrophage foam cells by truncation of the carboxyl terminus of apolipoprotein A-I. Parallel losses of pre-beta particles and the high affinity component of efflux. J. Biol. Chem., 1999, 274(32), 22627-22634.
[99]
Pirillo, A.; Ghiselli, G. Enhanced macrophage uptake of elastase-modified high-density lipoproteins. Biochem. Biophys. Res. Commun., 2000, 271(2), 386-391.
[100]
Gauster, M.; Oskolkova, O.V.; Innerlohinger, J.; Glatter, O.; Knipping, G.; Frank, S. Endothelial lipase-modified high-density lipoprotein exhibits diminished ability to mediate SR-BI (scavenger receptor B type I)-dependent free-cholesterol efflux. Biochem. J., 2004, 382(Pt 1), 75-82.
[101]
Van Lenten, B.J.; Hama, S.Y.; de Beer, F.C.; Stafforini, D.M.; McIntyre, T.M.; Prescott, S.M.; La Du, B.N.; Fogelman, A.M.; Navab, M. Anti-inflammatory HDL becomes pro-inflammatory during the acute phase response. Loss of protective effect of HDL against LDL oxidation in aortic wall cell cocultures. J. Clin. Invest., 1995, 96(6), 2758-2767.
[102]
Chen, Y.D.; Jeng, C.Y.; Reaven, G.M. HDL metabolism in diabetes. Diabetes Metab. Rev., 1987, 3(3), 653-668.
[103]
Ferretti, G.; Bacchetti, T.; Marchionni, C.; Caldarelli, L.; Curatola, G. Effect of glycation of high density lipoproteins on their physicochemical properties and on paraoxonase activity. Acta Diabetol., 2001, 38(4), 163-169.
[104]
Hedrick, C.C.; Thorpe, S.R.; Fu, M.X.; Harper, C.M.; Yoo, J.; Kim, S.M.; Wong, H.; Peters, A.L. Glycation impairs high-density lipoprotein function. Diabetologia, 2000, 43(3), 312-320.
[105]
Witztum, J.L.; Fisher, M.; Pietro, T.; Steinbrecher, U.P.; Elam, R.L. Nonenzymatic glucosylation of high-density lipoprotein accelerates its catabolism in guinea pigs. Diabetes, 1982, 31(11), 1029-1032.
[106]
Duell, P.B.; Oram, J.F.; Bierman, E.L. Nonenzymatic glycosylation of HDL resulting in inhibition of high-affinity binding to cultured human fibroblasts. Diabetes, 1990, 39(10), 1257-1263.
[107]
Duell, P.B.; Oram, J.F.; Bierman, E.L. Nonenzymatic glycosylation of HDL and impaired HDL-receptor-mediated cholesterol efflux. Diabetes, 1991, 40(3), 377-384.
[108]
Riwanto, M.; Rohrer, L.; Roschitzki, B.; Besler, C.; Mocharla, P.; Mueller, M.; Perisa, D.; Heinrich, K.; Altwegg, L.; von Eckardstein, A.; Lüscher, T.F.; Landmesser, U. Altered activation of endothelial anti- and proapoptotic pathways by high-density lipoprotein from patients with coronary artery disease: role of high-density lipoprotein-proteome remodeling. Circulation, 2013, 127(8), 891-904.
[109]
Beg, Z.H.; Stonik, J.A.; Hoeg, J.M.; Demosky, S.J., Jr; Fairwell, T.; Brewer, H.B., Jr Human apolipoprotein A-I. Post-translational modification by covalent phosphorylation. J. Biol. Chem., 1989, 264(12), 6913-6921.
[110]
Hoeg, J.M.; Meng, M.S.; Ronan, R.; Fairwell, T.; Brewer, H.B., Jr Human apolipoprotein A-I. Post-translational modification by fatty acid acylation. J. Biol. Chem., 1986, 261(9), 3911-3914.
[111]
Fernández-Irigoyen, J.; Santamaría, E.; Sesma, L.; Muñoz, J.; Riezu, J.I.; Caballería, J.; Lu, S.C.; Prieto, J.; Mato, J.M.; Avila, M.A.; Corrales, F.J. Oxidation of specific methionine and tryptophan residues of apolipoprotein A-I in hepatocarcinogenesis. Proteomics, 2005, 5(18), 4964-4972.
[112]
Vivanco, F.; Martín-Ventura, J.L.; Duran, M.C.; Barderas, M.G.; Blanco-Colio, L.; Dardé, V.M.; Mas, S.; Meilhac, O.; Michel, J.B.; Tuñón, J.; Egido, J. Quest for novel cardiovascular biomarkers by proteomic analysis. J. Proteome Res., 2005, 4(4), 1181-1191.
[113]
Erqou, S.; Thompson, A.; Di Angelantonio, E.; Saleheen, D.; Kaptoge, S.; Marcovina, S.; Danesh, J. Apolipoprotein(a) isoforms and the risk of vascular disease: systematic review of 40 studies involving 58,000 participants. J. Am. Coll. Cardiol., 2010, 55(19), 2160-2167.
[114]
Erqou, S.; Kaptoge, S.; Perry, P.L.; Di Angelantonio, E.; Thompson, A.; White, I.R.; Marcovina, S.M.; Collins, R.; Thompson, S.G.; Danesh, J. Emerging Risk Factors Collaboration. Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA, 2009, 302(4), 412-423.
[115]
Hopewell, J.C.; Seedorf, U.; Farrall, M.; Parish, S.; Kyriakou, T.; Goel, A.; Hamsten, A.; Collins, R.; Watkins, H.; Clarke, R. PROCARDIS Consortium. Impact of lipoprotein(a) levels and apolipoprotein(a) isoform size on risk of coronary heart disease. J. Intern. Med., 2014, 276(3), 260-268.
[116]
Kronenberg, F.; Utermann, G. Lipoprotein(a): resurrected by genetics. J. Intern. Med., 2013, 273(1), 6-30.
[117]
Laschkolnig, A.; Kollerits, B.; Lamina, C.; Meisinger, C.; Rantner, B.; Stadler, M.; Peters, A.; Koenig, W.; Stöckl, A.; Dähnhardt, D.; Böger, C.A.; Krämer, B.K.; Fraedrich, G.; Strauch, K.; Kronenberg, F. Lipoprotein (a) concentrations, apolipoprotein (a) phenotypes, and peripheral arterial disease in three independent cohorts. Cardiovasc. Res., 2014, 103(1), 28-36.
[118]
Kamstrup, P.R.; Tybjærg-Hansen, A.; Nordestgaard, B.G. Elevated lipoprotein(a) and risk of aortic valve stenosis in the general population. J. Am. Coll. Cardiol., 2014, 63(5), 470-477.
[119]
Capoulade, R.; Chan, K.L.; Yeang, C.; Mathieu, P.; Bossé, Y.; Dumesnil, J.G.; Tam, J.W.; Teo, K.K.; Mahmut, A.; Yang, X.; Witztum, J.L.; Arsenault, B.J.; Després, J.P.; Pibarot, P.; Tsimikas, S. Oxidized phospholipids, lipoprotein(a), and progression of calcific aortic valve stenosis. J. Am. Coll. Cardiol., 2015, 66(11), 1236-1246.
[120]
Koschinsky, M.L.; Boffa, M.B. Lipoprotein(a): an important cardiovascular risk factor and a clinical conundrum. Endocrinol. Metab. Clin. North Am., 2014, 43(4), 949-962.
[121]
Kelly, E.; Hemphill, L. Lipoprotein(a): A lipoprotein whose time has come. Curr. Treat. Options Cardiovasc. Med., 2017, 19(7), 48.
[122]
Tsimikas, S.; Brilakis, E.S.; Miller, E.R.; McConnell, J.P.; Lennon, R.J.; Kornman, K.S.; Witztum, J.L.; Berger, P.B. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease. N. Engl. J. Med., 2005, 353(1), 46-57.
[123]
Bergmark, C.; Dewan, A.; Orsoni, A.; Merki, E.; Miller, E.R.; Shin, M.J.; Binder, C.J.; Hörkkö, S.; Krauss, R.M.; Chapman, M.J.; Witztum, J.L.; Tsimikas, S. A novel function of lipoprotein [a] as a preferential carrier of oxidized phospholipids in human plasma. J. Lipid Res., 2008, 49(10), 2230-2239.
[124]
Marcovina, S.M.; Koschinsky, M.L. Evaluation of lipoprotein(a) as a prothrombotic factor: progress from bench to bedside. Curr. Opin. Lipidol., 2003, 14(4), 361-366.
[125]
Viney, N.J.; van Capelleveen, J.C.; Geary, R.S.; Xia, S.; Tami, J.A.; Yu, R.Z.; Marcovina, S.M.; Hughes, S.G.; Graham, M.J.; Crooke, R.M.; Crooke, S.T.; Witztum, J.L.; Stroes, E.S.; Tsimikas, S. Antisense oligonucleotides targeting apolipoprotein(a) in people with raised lipoprotein(a): two randomised, double-blind, placebo-controlled, dose-ranging trials. Lancet, 2016, 388(10057), 2239-2253.
[126]
Campbell, L.A.; Rosenfeld, M.E. Infection and atherosclerosis development. Arch. Med. Res., 2015, 46(5), 339-350.
[127]
Stary, H.C.; Chandler, A.B.; Glagov, S.; Guyton, J.R.; Insull, W., Jr; Rosenfeld, M.E.; Schaffer, S.A.; Schwartz, C.J.; Wagner, W.D.; Wissler, R.W. A definition of initial, fatty streak, and intermediate lesions of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation, 1994, 89(5), 2462-2478.
[128]
Jonasson, L.; Holm, J.; Skalli, O.; Bondjers, G.; Hansson, G.K. Regional accumulations of T cells, macrophages, and smooth muscle cells in the human atherosclerotic plaque. Arteriosclerosis, 1986, 6(2), 131-138.
[129]
Kovanen, P.T.; Kaartinen, M.; Paavonen, T. Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction. Circulation, 1995, 92(5), 1084-1088.
[130]
Gutstein, D.E.; Fuster, V. Pathophysiology and clinical significance of atherosclerotic plaque rupture. Cardiovasc. Res., 1999, 41(2), 323-333.
[131]
Ridker, P.M.; Rifai, N.; Rose, L.; Buring, J.E.; Cook, N.R. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. N. Engl. J. Med., 2002, 347(20), 1557-1565.
[132]
Stylianou, I.M.; Bauer, R.C.; Reilly, M.P.; Rader, D.J. Genetic basis of atherosclerosis: insights from mice and humans. Circ. Res., 2012, 110(2), 337-355.
[133]
Roberts, C.K.; Ng, C.; Hama, S.; Eliseo, A.J.; Barnard, R.J. Effect of a short-term diet and exercise intervention on inflammatory/anti-inflammatory properties of HDL in overweight/obese men with cardiovascular risk factors. J. Appl. Physiol., 2006, 101(6), 1727-1732.
[134]
Navab, M.; Anantharamaiah, G.M.; Reddy, S.T.; Hama, S.; Hough, G.; Grijalva, V.R.; Wagner, A.C.; Frank, J.S.; Datta, G.; Garber, D.; Fogelman, A.M. Oral D-4F causes formation of pre-beta high-density lipoprotein and improves high-density lipoprotein-mediated cholesterol efflux and reverse cholesterol transport from macrophages in apolipoprotein E-null mice. Circulation, 2004, 109(25), 3215-3220.
[135]
Cockerill, G.W.; Rye, K.A.; Gamble, J.R.; Vadas, M.A.; Barter, P.J. High-density lipoproteins inhibit cytokine-induced expression of endothelial cell adhesion molecules. Arterioscler. Thromb. Vasc. Biol., 1995, 15(11), 1987-1994.
[136]
Baker, P.W.; Rye, K.A.; Gamble, J.R.; Vadas, M.A.; Barter, P.J. Ability of reconstituted high density lipoproteins to inhibit cytokine-induced expression of vascular cell adhesion molecule-1 in human umbilical vein endothelial cells. J. Lipid Res., 1999, 40(2), 345-353.
[137]
Nofer, J.R.; Assmann, G. Atheroprotective effects of high-density lipoprotein-associated lysosphingolipids. Trends Cardiovasc. Med., 2005, 15(7), 265-271.
[138]
Robbesyn, F.; Garcia, V.; Auge, N.; Vieira, O.; Frisach, M.F.; Salvayre, R.; Negre-Salvayre, A. HDL counterbalance the proinflammatory effect of oxidized LDL by inhibiting intracellular reactive oxygen species rise, proteasome activation, and subsequent NF-kappa B activation in smooth muscle cells. FASEB J., 2003, 17(6), 743-745.
[139]
Xia, P.; Vadas, M.A.; Rye, K.A.; Barter, P.J.; Gamble, J.R. High density lipoproteins (HDL) interrupt the sphingosine kinase signaling pathway. A possible mechanism for protection against atherosclerosis by HDL. J. Biol. Chem., 1999, 274(46), 33143-33147.
[140]
Barter, P.J.; Baker, P.W.; Rye, K.A. Effect of high-density lipoproteins on the expression of adhesion molecules in endothelial cells. Curr. Opin. Lipidol., 2002, 13(3), 285-288.
[141]
Sugatani, J.; Miwa, M.; Komiyama, Y.; Ito, S. High-density lipoprotein inhibits the synthesis of platelet-activating factor in human vascular endothelial cells. J. Lipid Mediat. Cell Signal., 1996, 13(1), 73-88.
[142]
Wadham, C.; Albanese, N.; Roberts, J.; Wang, L.; Bagley, C.J.; Gamble, J.R.; Rye, K.A.; Barter, P.J.; Vadas, M.A.; Xia, P. High-density lipoproteins neutralize C-reactive protein proinflammatory activity. Circulation, 2004, 109(17), 2116-2122.
[143]
Furnkranz, A.; Schober, A.; Bochkov, V.N.; Bashtrykov, P.; Kronke, G.; Kadl, A.; Binder, B.R.; Weber, C.; Leitinger, N. Oxidized phospholipids trigger atherogenic inflammation in murine arteries. Arterioscler. Thromb. Vasc. Biol., 2005, 25(3), 633-638.
[144]
Stary, H.C. Natural history and histological classification of atherosclerotic lesions: an update. Arterioscler. Thromb. Vasc. Biol., 2000, 20(5), 1177-1178.
[145]
Virmani, R.; Kolodgie, F.D.; Burke, A.P.; Farb, A.; Schwartz, S.M. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler. Thromb. Vasc. Biol., 2000, 20(5), 1262-1275.
[146]
Hansson, G.K.; Hermansson, A. The immune system in atherosclerosis. Nat. Immunol., 2011, 12(3), 204-212.
[147]
Simionescu, M. Implications of early structural-functional changes in the endothelium for vascular disease. Arterioscler. Thromb. Vasc. Biol., 2007, 27(2), 266-274.
[148]
Simionescu, M.; Popov, D.; Sima, A. Endothelial transcytosis in health and disease. Cell Tissue Res., 2009, 335(1), 27-40.
[149]
Simionescu, M.; Simionescu, N.; Silbert, J.E.; Palade, G.E. Differentiated microdomains on the luminal surface of the capillary endothelium. II. Partial characterization of their anionic sites. J. Cell Biol., 1981, 90(3), 614-621.
[150]
Gimbrone, M.A., Jr; García-Cardeña, G. Endothelial cell dysfunction and the pathobiology of atherosclerosis. Circ. Res., 2016, 118(4), 620-636.
[151]
Simionescu, N.; Vasile, E.; Lupu, F.; Popescu, G.; Simionescu, M. Prelesional events in atherogenesis. Accumulation of extracellular cholesterol-rich liposomes in the arterial intima and cardiac valves of the hyperlipidemic rabbit. Am. J. Pathol., 1986, 123(1), 109-125.
[152]
Simionescu, N.; Mora, R.; Vasile, E.; Lupu, F.; Filip, D.A.; Simionescu, M. Prelesional modifications of the vessel wall in hyperlipidemic atherogenesis. Extracellular accumulation of modified and reassembled lipoproteins. Ann. N. Y. Acad. Sci., 1990, 598, 1-16.
[153]
Kakutani, M.; Masaki, T.; Sawamura, T. A platelet-endothelium interaction mediated by lectin-like oxidized low-density lipoprotein receptor-1. Proc. Natl. Acad. Sci. USA, 2000, 97(1), 360-364.
[154]
Mukherjee, S.; Coaxum, S.D.; Maleque, M.; Das, S.K. Effects of oxidized low density lipoprotein on nitric oxide synthetase and protein kinase C activities in bovine endothelial cells. Cell. Mol. Biol., 2001, 47(6), 1051-1058.
[155]
Rosenfeld, M.E.; Campbell, L.A. Pathogens and atherosclerosis: update on the potential contribution of multiple infectious organisms to the pathogenesis of atherosclerosis. Thromb. Haemost., 2011, 106(5), 858-867.
[156]
Kuo, C.C.; Shor, A.; Campbell, L.A.; Fukushi, H.; Patton, D.L.; Grayston, J.T. Demonstration of Chlamydia pneumoniae in atherosclerotic lesions of coronary arteries. J. Infect. Dis., 1993, 167(4), 841-849.
[157]
Campbell, L.A.; O’Brien, E.R.; Cappuccio, A.L.; Kuo, C.C.; Wang, S.P.; Stewart, D.; Patton, D.L.; Cummings, P.K.; Grayston, J.T. Detection of Chlamydia pneumoniae TWAR in human coronary atherectomy tissues. J. Infect. Dis., 1995, 172(2), 585-588.
[158]
Shor, A.; Kuo, C.C.; Patton, D.L. Detection of Chlamydia pneumoniae in coronary arterial fatty streaks and atheromatous plaques. S. Afr. Med. J., 1992, 82(3), 158-161.
[159]
Chiu, B. Multiple infections in carotid atherosclerotic plaques. Am. Heart J., 1999, 138(5 Pt 2), S534-S536.
[160]
Ford, P.J.; Gemmell, E.; Chan, A.; Carter, C.L.; Walker, P.J.; Bird, P.S.; West, M.J.; Cullinan, M.P.; Seymour, G.J. Inflammation, heat shock proteins and periodontal pathogens in atherosclerosis: an immunohistologic study. Oral Microbiol. Immunol., 2006, 21(4), 206-211.
[161]
Haraszthy, V.I.; Zambon, J.J.; Trevisan, M.; Zeid, M.; Genco, R.J. Identification of periodontal pathogens in atheromatous plaques. J. Periodontol., 2000, 71(10), 1554-1560.
[162]
Reszka, E.; Jegier, B.; Wasowicz, W.; Lelonek, M.; Banach, M.; Jaszewski, R. Detection of infectious agents by polymerase chain reaction in human aortic wall. Cardiovasc. Pathol., 2008, 17(5), 297-302.
[163]
Latsios, G.; Saetta, A.; Michalopoulos, N.V.; Agapitos, E.; Patsouris, E. Detection of cytomegalovirus, Helicobacter pylori and Chlamydia pneumoniae DNA in carotid atherosclerotic plaques by the polymerase chain reaction. Acta Cardiol., 2004, 59(6), 652-657.
[164]
Pucar, A.; Milasin, J.; Lekovic, V.; Vukadinovic, M.; Ristic, M.; Putnik, S.; Kenney, E.B. Correlation between atherosclerosis and periodontal putative pathogenic bacterial infections in coronary and internal mammary arteries. J. Periodontol., 2007, 78(4), 677-682.
[165]
Rose, J.R.; Mullarkey, M.A.; Christ, W.J.; Hawkins, L.D.; Lynn, M.; Kishi, Y.; Wasan, K.M.; Peteherych, K.; Rossignol, D.P. Consequences of interaction of a lipophilic endotoxin antagonist with plasma lipoproteins. Antimicrob. Agents Chemother., 2000, 44(3), 504-510.
[166]
Murch, O.; Collin, M.; Hinds, C.J.; Thiemermann, C. Lipoproteins in inflammation and sepsis. I. Basic science. Intensive Care Med., 2007, 33(1), 13-24.
[167]
Poelvoorde, P.; Vanhamme, L.; Van Den Abbeele, J.; Switzer, W.M.; Pays, E. Distribution of apolipoprotein L-I and trypanosome lytic activity among primate sera. Mol. Biochem. Parasitol., 2004, 134(1), 155-157.
[168]
Gabay, C.; Kushner, I. Acute-phase proteins and other systemic responses to inflammation. N. Engl. J. Med., 1999, 340(6), 448-454.
[169]
Thaveeratitham, P.; Khovidhunkit, W.; Patumraj, S. High-density lipoproteins (HDL) inhibit endotoxin-induced leukocyte adhesion on endothelial cells in rats: effect of the acute-phase HDL. Clin. Hemorheol. Microcirc., 2007, 36(1), 1-12.
[170]
Berbée, J.F.; van der Hoogt, C.C.; Kleemann, R.; Schippers, E.F.; Kitchens, R.L.; van Dissel, J.T.; Bakker-Woudenberg, I.A.; Havekes, L.M.; Rensen, P.C. Apolipoprotein CI stimulates the response to lipopolysaccharide and reduces mortality in gram-negative sepsis. FASEB J., 2006, 20(12), 2162-2164.
[171]
Nicholls, S.J.; Lundman, P.; Harmer, J.A.; Cutri, B.; Griffiths, K.A.; Rye, K.A.; Barter, P.J.; Celermajer, D.S. Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function. J. Am. Coll. Cardiol., 2006, 48(4), 715-720.
[172]
Tall, A.R.; Yvan-Charvet, L.; Wang, N. The failure of torcetrapib: was it the molecule or the mechanism? Arterioscler. Thromb. Vasc. Biol., 2007, 27(2), 257-260.
[173]
Ansell, B.J.; Navab, M.; Hama, S.; Kamranpour, N.; Fonarow, G.; Hough, G.; Rahmani, S.; Mottahedeh, R.; Dave, R.; Reddy, S.T.; Fogelman, A.M. Inflammatory/antiinflammatory properties of high-density lipoprotein distinguish patients from control subjects better than high-density lipoprotein cholesterol levels and are favorably affected by simvastatin treatment. Circulation, 2003, 108(22), 2751-2756.
[174]
Navab, M.; Ananthramaiah, G.M.; Reddy, S.T.; Van Lenten, B.J.; Ansell, B.J.; Hama, S.; Hough, G.; Bachini, E.; Grijalva, V.R.; Wagner, A.C.; Shaposhnik, Z.; Fogelman, A.M. The double jeopardy of HDL. Ann. Med., 2005, 37(3), 173-178.
[175]
Huang, Y.; DiDonato, J.A.; Levison, B. S.; Schmitt, D.; Li, L.; Wu, Y.; Buffa, J.; Kim, T.; Gerstenecker, G. S.; Gu, X.; Kadiyala, C. S.; Wang, Z.; Culley, M. K.; Hazen, J. E.; Didonato, A. J.; Fu, X.; Berisha, S. Z.; Peng, D.; Nguyen,donato, A. J.; Fu, X.; Berisha, S. Z.; Peng, D.; Nguyen, T. T.; Liang, S.; Chuang, C. C.; Cho, L.; Plow, E. F.; Fox, P. L.; Gogonea, V.; Tang, W. H.; Parks, J. S.; Fisher, E. A.; Smith, J. D.; Hazen, S. L An abundant dysfunctional apolipoprotein A1 in human atheroma. Nat. Med., 2014, 20(2), 193-203.
[176]
Roberts, C.K.; Ng, C.; Hama, S.; Eliseo, A.J.; Barnard, R.J. Effect of a short-term diet and exercise intervention on inflammatory/anti-inflammatory properties of HDL in overweight/obese men with cardiovascular risk factors. J. Appl. Physiol., 2006, 101(6), 1727-1732.
[177]
Sirtori, C.R.; Calabresi, L.; Franceschini, G.; Baldassarre, D.; Amato, M.; Johansson, J.; Salvetti, M.; Monteduro, C.; Zulli, R.; Muiesan, M.L.; Agabiti-Rosei, E. Cardiovascular status of carriers of the apolipoprotein A-I(Milano) mutant: the Limone sul Garda study. Circulation, 2001, 103(15), 1949-1954.
[178]
Wolfrum, C.; Poy, M.N.; Stoffel, M. Apolipoprotein M is required for prebeta-HDL formation and cholesterol efflux to HDL and protects against atherosclerosis. Nat. Med., 2005, 11(4), 418-422.
[179]
Christoffersen, C.; Nielsen, L.B.; Axler, O.; Andersson, A.; Johnsen, A.H.; Dahlbäck, B. Isolation and characterization of human apolipoprotein M-containing lipoproteins. J. Lipid Res., 2006, 47(8), 1833-1843.
[180]
Imaizumi, S.; Navab, M.; Morgantini, C.; Charles-Schoeman, C.; Su, F.; Gao, F.; Kwon, M.; Ganapathy, E.; Meriwether, D.; Farias-Eisner, R.; Fogelman, A.M.; Reddy, S.T. Dysfunctional high-density lipoprotein and the potential of apolipoprotein A-1 mimetic peptides to normalize the composition and function of lipoproteins. Circ. J., 2011, 75(7), 1533-1538.
Related Journals
Current Pharmaceutical Design
Current Topics in Medicinal Chemistry
Current Respiratory Medicine Reviews
Infectious Disorders - Drug Targets
Endocrine, Metabolic & Immune Disorders - Drug Targets
Anti-Infective Agents
Coronaviruses
Recent Advances in Inflammation & Allergy Drug Discovery
Current Probiotics
Article Metrics
52
8
1