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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
MeSH Review

Foam Cells

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Disease relevance of Foam Cells


High impact information on Foam Cells


Chemical compound and disease context of Foam Cells

  • The findings suggest the hypothetical but intriguing possibility that probucol, in addition to its recognized effects on plasma LDL levels, may inhibit atherogenesis by limiting oxidative LDL modification and thus foam cell formation and/or EC injury [9].
  • Recent studies have shown that oestrogen, progesterone and androgens all regulate processes integral to human macrophage foam cell formation, a key event in atherogenesis, in a sex-specific manner; findings that may have important implications for understanding the sex gap in atherosclerosis [10].
  • The macrophage scavenger receptor, a 220-kDa trimeric membrane glycoprotein, mediates the internalization of modified forms of low density lipoprotein (LDL) such as acetyl-LDL and oxidized-LDL and thus is likely to play a key role in atheroma macrophage foam cell formation [11].
  • It therefore seems unlikely that the beneficial effect of atenolol on coronary heart disease is mediated by changes in either LDL oxidizability or cholesterol metabolism in human macrophages and foam cells [12].
  • These results suggest that under atherogenic conditions, macrophages release proteoglycans, and mainly chondroitin sulfate, which can contribute to cell-mediated formation of aggregated LDL, a potent inducer of macrophage foam cells which are the hallmark of early atherogenesis [13].

Biological context of Foam Cells

  • The enhancement of SCP2 gene expression by AcLDL suggests that SCP2 may play an important role during foam cell formation induced by AcLDL which may be most important step for the atherosclerosis [14].
  • Histology and morphometry, physical microscopy for cholesterol monohydrate crystals, foam cell and droplet melting points and chemical composition studies were completed on a large number of individual arterial lesions [15].
  • Herein we identify adipocyte enhancer-binding protein 1 (AEBP1) as a transcriptional repressor that impedes macrophage cholesterol efflux, promoting foam cell formation, via PPARgamma1 and LXRalpha down-regulation [16].
  • Macrophages in atherosclerotic lesions accumulate large amounts of cholesteryl-fatty acyl esters ("foam cell" formation) through the intracellular esterification of cholesterol by acyl-coenzyme A:cholesterol O-acyltransferase (ACAT) [17].
  • In these cells, CD36 is involved in phagocytosis of apoptotic cells, and foam cell formation by uptake of oxidized low density lipoprotein [18].

Anatomical context of Foam Cells


Associations of Foam Cells with chemical compounds

  • Histologically, lesions in probucol-treated mice contained increased fibrous materials and cells other than foam cells, and were commonly associated with focal inflammation and aneurysmal dilatation [24].
  • These data suggest that: (a) the shellfish sterols desmosterol and 24-methylene cholesterol may be atherogenic; and (b) the excessive foam cell formation seen in sitosterolemia and CTX cannot be explained by ACAT hyperreactivity of their associated sterols [25].
  • Immunohistochemical studies confirmed that foam cells adjacent to the lipid necrotic core of the plaque were markedly positive for 8-epi PGF2alpha [26].
  • If overwhelmed, foam cell formation, endothelial dysfunction, and atherothrombogenesis may ensue, a mechanism for cardiovascular disease risk of elevated TG [27].
  • In some regions of the thickened intima, foam cells accumulate along the luminal margin [28].

Gene context of Foam Cells

  • To investigate the potential importance of these activities in vivo, we performed a systematic analysis of the effects of PPARalpha, beta, and gamma agonists on foam-cell formation and atherosclerosis in male LDL receptor-deficient (LDLR(-/-)) mice [29].
  • In conclusion, these studies show a very low expression of LPL mRNA in the CD14-positive macrophage-derived foam cells isolated from human atherosclerotic tissue [30].
  • These data demonstrate that in selected models of murine atherosclerosis, chronic IL-1ra depletion or overexpression has potentially important effects on lipoprotein metabolism and foam-cell lesion development [31].
  • In summary, in foam cells during atherosclerosis regression, there is induction of CCR7 and a requirement for its function [32].
  • Regulated expression of CD36 during monocyte-to-macrophage differentiation: potential role of CD36 in foam cell formation [33].

Analytical, diagnostic and therapeutic context of Foam Cells


  1. Tangier disease is caused by mutations in the gene encoding ATP-binding cassette transporter 1. Rust, S., Rosier, M., Funke, H., Real, J., Amoura, Z., Piette, J.C., Deleuze, J.F., Brewer, H.B., Duverger, N., Denèfle, P., Assmann, G. Nat. Genet. (1999) [Pubmed]
  2. Malondialdehyde-altered protein occurs in atheroma of Watanabe heritable hyperlipidemic rabbits. Haberland, M.E., Fong, D., Cheng, L. Science (1988) [Pubmed]
  3. Macrophages from nephrotic rats regulate apolipoprotein E biosynthesis and cholesterol content independently. Bass, J., Fisher, E.A., Prack, M.M., Williams, D.L., Marsh, J.B. J. Clin. Invest. (1991) [Pubmed]
  4. HIV protease inhibitors promote atherosclerotic lesion formation independent of dyslipidemia by increasing CD36-dependent cholesteryl ester accumulation in macrophages. Dressman, J., Kincer, J., Matveev, S.V., Guo, L., Greenberg, R.N., Guerin, T., Meade, D., Li, X.A., Zhu, W., Uittenbogaard, A., Wilson, M.E., Smart, E.J. J. Clin. Invest. (2003) [Pubmed]
  5. Emerging role of myeloperoxidase and oxidant stress markers in cardiovascular risk assessment. Brennan, M.L., Hazen, S.L. Curr. Opin. Lipidol. (2003) [Pubmed]
  6. PPAR-alpha and PPAR-gamma activators induce cholesterol removal from human macrophage foam cells through stimulation of the ABCA1 pathway. Chinetti, G., Lestavel, S., Bocher, V., Remaley, A.T., Neve, B., Torra, I.P., Teissier, E., Minnich, A., Jaye, M., Duverger, N., Brewer, H.B., Fruchart, J.C., Clavey, V., Staels, B. Nat. Med. (2001) [Pubmed]
  7. The role of PPAR-gamma in macrophage differentiation and cholesterol uptake. Moore, K.J., Rosen, E.D., Fitzgerald, M.L., Randow, F., Andersson, L.P., Altshuler, D., Milstone, D.S., Mortensen, R.M., Spiegelman, B.M., Freeman, M.W. Nat. Med. (2001) [Pubmed]
  8. Interdomain communication regulating ligand binding by PPAR-gamma. Shao, D., Rangwala, S.M., Bailey, S.T., Krakow, S.L., Reginato, M.J., Lazar, M.A. Nature (1998) [Pubmed]
  9. Probucol inhibits oxidative modification of low density lipoprotein. Parthasarathy, S., Young, S.G., Witztum, J.L., Pittman, R.C., Steinberg, D. J. Clin. Invest. (1986) [Pubmed]
  10. Sex-related differences in the regulation of macrophage cholesterol metabolism. Ng, M.K., Jessup, W., Celermajer, D.S. Curr. Opin. Lipidol. (2001) [Pubmed]
  11. Transforming growth factor-beta 1 inhibits scavenger receptor activity in THP-1 human macrophages. Bottalico, L.A., Wager, R.E., Agellon, L.B., Assoian, R.K., Tabas, I. J. Biol. Chem. (1991) [Pubmed]
  12. Impact of a combination of a calcium antagonist and a beta-blocker on cell- and copper-mediated oxidation of LDL and on the accumulation and efflux of cholesterol in human macrophages and murine J774 cells. Lesnik, P., Dachet, C., Petit, L., Moreau, M., Griglio, S., Brudi, P., Chapman, M.J. Arterioscler. Thromb. Vasc. Biol. (1997) [Pubmed]
  13. Macrophage released proteoglycans are involved in cell-mediated aggregation of LDL. Maor, I., Aviram, M. Atherosclerosis (1999) [Pubmed]
  14. Regulation of sterol carrier protein 2 (SCP2) gene expression in rat peritoneal macrophages during foam cell formation. A key role for free cholesterol content. Hirai, A., Kino, T., Tokinaga, K., Tahara, K., Tamura, Y., Yoshida, S. J. Clin. Invest. (1994) [Pubmed]
  15. Physicochemical and histological changes in the arterial wall of nonhuman primates during progression and regression of atherosclerosis. Small, D.M., Bond, M.G., Waugh, D., Prack, M., Sawyer, J.K. J. Clin. Invest. (1984) [Pubmed]
  16. Adipocyte enhancer-binding protein 1 is a potential novel atherogenic factor involved in macrophage cholesterol homeostasis and inflammation. Majdalawieh, A., Zhang, L., Fuki, I.V., Rader, D.J., Ro, H.S. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  17. Immunolocalization of acyl-coenzyme A:cholesterol O-acyltransferase in macrophages. Khelef, N., Buton, X., Beatini, N., Wang, H., Meiner, V., Chang, T.Y., Farese, R.V., Maxfield, F.R., Tabas, I. J. Biol. Chem. (1998) [Pubmed]
  18. Structural and functional characterization of the human CD36 gene promoter: identification of a proximal PEBP2/CBF site. Armesilla, A.L., Calvo, D., Vega, M.A. J. Biol. Chem. (1996) [Pubmed]
  19. Macrophage-colony-stimulating factor selectively enhances macrophage scavenger receptor expression and function. de Villiers, W.J., Fraser, I.P., Hughes, D.A., Doyle, A.G., Gordon, S. J. Exp. Med. (1994) [Pubmed]
  20. Lipoprotein lipase is synthesized by macrophage-derived foam cells in human coronary atherosclerotic plaques. O'Brien, K.D., Gordon, D., Deeb, S., Ferguson, M., Chait, A. J. Clin. Invest. (1992) [Pubmed]
  21. Apo A-I inhibits foam cell formation in Apo E-deficient mice after monocyte adherence to endothelium. Dansky, H.M., Charlton, S.A., Barlow, C.B., Tamminen, M., Smith, J.D., Frank, J.S., Breslow, J.L. J. Clin. Invest. (1999) [Pubmed]
  22. Stimulated arachidonate metabolism during foam cell transformation of mouse peritoneal macrophages with oxidized low density lipoprotein. Yokode, M., Kita, T., Kikawa, Y., Ogorochi, T., Narumiya, S., Kawai, C. J. Clin. Invest. (1988) [Pubmed]
  23. Chymase in exocytosed rat mast cell granules effectively proteolyzes apolipoprotein AI-containing lipoproteins, so reducing the cholesterol efflux-inducing ability of serum and aortic intimal fluid. Lindstedt, L., Lee, M., Castro, G.R., Fruchart, J.C., Kovanen, P.T. J. Clin. Invest. (1996) [Pubmed]
  24. Paradoxical enhancement of atherosclerosis by probucol treatment in apolipoprotein E-deficient mice. Zhang, S.H., Reddick, R.L., Avdievich, E., Surles, L.K., Jones, R.G., Reynolds, J.B., Quarfordt, S.H., Maeda, N. J. Clin. Invest. (1997) [Pubmed]
  25. The reactivity of desmosterol and other shellfish- and xanthomatosis-associated sterols in the macrophage sterol esterification reaction. Tabas, I., Feinmark, S.J., Beatini, N. J. Clin. Invest. (1989) [Pubmed]
  26. Localization of distinct F2-isoprostanes in human atherosclerotic lesions. Praticò, D., Iuliano, L., Mauriello, A., Spagnoli, L., Lawson, J.A., Rokach, J., Maclouf, J., Violi, F., FitzGerald, G.A. J. Clin. Invest. (1997) [Pubmed]
  27. A macrophage receptor for apolipoprotein B48: cloning, expression, and atherosclerosis. Brown, M.L., Ramprasad, M.P., Umeda, P.K., Tanaka, A., Kobayashi, Y., Watanabe, T., Shimoyamada, H., Kuo, W.L., Li, R., Song, R., Bradley, W.A., Gianturco, S.H. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  28. Luminal foam cell accumulation is associated with smooth muscle cell death in the intimal thickening of human saphenous vein grafts. Kockx, M.M., De Meyer, G.R., Bortier, H., de Meyere, N., Muhring, J., Bakker, A., Jacob, W., Van Vaeck, L., Herman, A. Circulation (1996) [Pubmed]
  29. Differential inhibition of macrophage foam-cell formation and atherosclerosis in mice by PPARalpha, beta/delta, and gamma. Li, A.C., Binder, C.J., Gutierrez, A., Brown, K.K., Plotkin, C.R., Pattison, J.W., Valledor, A.F., Davis, R.A., Willson, T.M., Witztum, J.L., Palinski, W., Glass, C.K. J. Clin. Invest. (2004) [Pubmed]
  30. Expression of lipoprotein lipase mRNA and secretion in macrophages isolated from human atherosclerotic aorta. Mattsson, L., Johansson, H., Ottosson, M., Bondjers, G., Wiklund, O. J. Clin. Invest. (1993) [Pubmed]
  31. Genetic alterations of IL-1 receptor antagonist in mice affect plasma cholesterol level and foam cell lesion size. Devlin, C.M., Kuriakose, G., Hirsch, E., Tabas, I. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  32. Gene expression changes in foam cells and the role of chemokine receptor CCR7 during atherosclerosis regression in ApoE-deficient mice. Trogan, E., Feig, J.E., Dogan, S., Rothblat, G.H., Angeli, V., Tacke, F., Randolph, G.J., Fisher, E.A. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  33. Regulated expression of CD36 during monocyte-to-macrophage differentiation: potential role of CD36 in foam cell formation. Huh, H.Y., Pearce, S.F., Yesner, L.M., Schindler, J.L., Silverstein, R.L. Blood (1996) [Pubmed]
  34. Macrophages and smooth muscle cells express lipoprotein lipase in human and rabbit atherosclerotic lesions. Ylä-Herttuala, S., Lipton, B.A., Rosenfeld, M.E., Goldberg, I.J., Steinberg, D., Witztum, J.L. Proc. Natl. Acad. Sci. U.S.A. (1991) [Pubmed]
  35. Retroviral gene therapy in ApoE-deficient mice: ApoE expression in the artery wall reduces early foam cell lesion formation. Hasty, A.H., Linton, M.F., Brandt, S.J., Babaev, V.R., Gleaves, L.A., Fazio, S. Circulation (1999) [Pubmed]
  36. Evolution of foam cells in subcutaneous rabbit carrageenan granulomas: I. Light-microscopic and ultrastructural study. Schwartz, C.J., Ghidoni, J.J., Kelley, J.L., Sprague, E.A., Valente, A.J., Suenram, C.A. Am. J. Pathol. (1985) [Pubmed]
  37. Expression of heme oxygenase-1 in atherosclerotic lesions. Wang, L.J., Lee, T.S., Lee, F.Y., Pai, R.C., Chau, L.Y. Am. J. Pathol. (1998) [Pubmed]
  38. The apolipoprotein e knockout mouse: a model documenting accelerated atherogenesis in uremia. Buzello, M., Törnig, J., Faulhaber, J., Ehmke, H., Ritz, E., Amann, K. J. Am. Soc. Nephrol. (2003) [Pubmed]
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