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Cholesterol Podcasts. Arterioscler Thromb Vasc Biol ; 23 : — Barter P. Metabolic abnormalities: high-density lipoproteins.

Endocrinol Metab Clin North Am ; 33 : — Cholesteryl ester transfer protein: a novel target for raising HDL and inhibiting atherosclerosis.

Elevation of plasma high-density lipoprotein concentration reduces interleukininduced expression of E-selectin in an in vivo model of acute inflammation. Circulation ; : — High-density lipoproteins differentially modulate cytokine-induced expression of E-selectin and cyclooxygenase Arterioscler Thromb Vasc Biol ; 19 : — High-density lipoproteins inhibit cytokine-induced expression of endothelial cell adhesion molecules.

Arterioscler Thromb Vasc Biol ; 15 : — Time sequence of the inhibition of endothelial adhesion molecule expression by reconstituted high density lipoproteins.

Atherosclerosis ; : 23 — Reconstituted high density lipoprotein modulates adherence of polymorphonuclear leukocytes to human endothelial cells. Shock ; 7 : — High density lipoprotein-associated lysosphingolipids reduce E-selectin expression in human endothelial cells. Biochem Biophys Res Commun ; : 98 — Mechanisms of high-density lipoprotein cholesterol effects on the endothelial function in hyperlipemia.

Metabolism ; 52 : — Effects of hypolipidemic treatment on serum markers of vascular inflammation in dyslipidemic men. Elevated soluble cellular adhesion molecules in subjects with low HDL-cholesterol. Arterioscler Thromb Vasc Biol ; 22 : — High density lipoproteins HDL interrupt the sphingosine kinase signaling pathway.

A possible mechanism for protection against atherosclerosis by HDL. J Biol Chem ; : — High-density lipoproteins neutralize C-reactive protein proinflammatory activity. Biochem Biophys Res Commun ; : — 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 ; 88 : — Expression of the monocyte chemoattractant protein-1 receptor CCR2 is increased in hypercholesterolemia.

Differential effects of plasma lipoproteins on monocyte function. J Lipid Res ; 40 : — Thromb Res ; 70 : — Influence of HDL subfractions on erythrocyte aggregation in hypercholesterolemic men. Arterioscler Thromb ; 14 : — Arterioscler Thromb Vasc Biol ; 16 : — Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.

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Volume 7. Article Contents Abstract. Overview of lipid metabolism. Pathophysiology of atherogenesis. Anti-atherogenic properties of HDL-cholesterol. The role of HDL-cholesterol in preventing atherosclerotic disease. Philip Barter Philip Barter. E-mail address : p. Oxford Academic. Google Scholar.

Select Format Select format. Permissions Icon Permissions. Abstract The cholesterol required by peripheral tissues, including vascular cells, is provided both by new synthesis in the cells and by a delivery from low-density lipoproteins LDLs.

Open in new tab Download slide. Marchesi, and S. O'Brien, G. Watts, D. Playford, V. Burke, D. O'Neal, and J. Zhang, S. Zhao, X. Li, M. Gao, and QI. Conlan, A. Folsom, A. Finch, C. Davis, P. Sorlie, G. Marcucci, and K. View at: Google Scholar N. Boyd and V. Gospodarowicz, G. Lui, and R. Rotheneder and G. Nofer, R. Junker, and R. Levkau, and B. Knapp, S. Al-Sheibani, and P. Hoyer and G. Gaard, S. Tretli, and F. Bani, C.

Williams, P. Boulter, and J. Kokoglu, I. Karaarslan, H. Karaarslan, and H. Schreier, G. Berg, F. Basilio, G. Lopez, A. Etkin, and R. Ray and S. Furberg, M. Wilsgaard, L. Berstein, and I. View at: Google Scholar P. Moorman, B. Hulka, R. Hiatt, N. Krieger, B. Newman, J. Vogelman, and N. View at: Google Scholar K. Siemianowicz, J. Gminski, and J. View at: Google Scholar S. Dessi, B. Batetta, and B. Fiorenza, A. Branchi, and D. Kucharska-Newton, W. Rosamond, J. Schroeder, A.

McNeill, J. Coresh, and A. Ahn, U. Lim, S. Weinstein, A. Schatzkin, R. Hayes, J. Virtamo, and D. A31—A35, Von Eckardstein, M. Hersberger, and L. Esteve, W. Ricart, and J. Spiegel, E. Schaefer, I. Magrath, and B. Blackman, V. Cabana, and T. Lim, T. Gayles, and T. Navab, G. Ananthramaiah, and G. Tietge, C.

Maugeais, W. Cain, and D. E—E, View at: Google Scholar L. Spieker, F. Ruschitzka, T. Cockerill, T. Huehns, A. Weerasinghe, C. Stocker, P. Lerch, N. Miller, and D. Ansell, K. Watson, A. Fogelman, M. Navab, and G. Whitehouse, C. Sciulli, and R. View at: Google Scholar I. Martins, E. Hone, and E.

Xuereb, C. Brayne, and C. Eckert, C. Kirsch, S. Leutz, W. Wood, and W. Koudinov and N. Guglielmotto, L. Giliberto, E. Tamagno, and M. Dominique Ashen and R. Ward, C. Carlsson, M. Trivedi, M.

Sager, and S. Kramer, K. Erickson, and S. Barzilai, G. Atzmon, C. Derby, J. Bauman, and R. Singh-Manoux, D. Gimeno, M. Kivimaki, E. Brunner, and M. Wahrle, H. Jiang, and H. Olesen and L. Ming, and T. Hardy and K. Reiss, K. Siller, M. Rahman, E. Chan, J. Ghiso, and M. Wolf, A. Hensel, T.