Uptake of type III hypertriglyceridemic VLDL by macrophages is enhanced by oxidation, especially after remnant formation

Whitman, Stewart C.; Miller, David B.; Wolfe, Bernard M.; Hegele, Robert A.; Huff, Murray W.

doi:10.1161/01.atv.17.9.1707

Cited by 59Cholesterol and Lipid MetabolismAtherosclerosis and Cardiovascular DiseasesLipid metabolism and disorders

Uptake of type III hypertriglyceridemic VLDL by macrophages is enhanced by oxidation, especially after remnant formation

Open access

Whitman, Stewart C., Miller, David B., Wolfe, Bernard M., Hegele, Robert A., Huff, Murray W.·1997·Arteriosclerosis, Thrombosis, and Vascular Biology

DOI 10.1161/01.atv.17.9.1707

Open this paper in CoChat — free account Open PDF

Abstract

Abstract We previously showed that hypertriglyceridemic VLDL (HTG-VLDL, Sf 60 to 400) from subjects with type III (E2/E2) hyperlipoproteinemia do not induce appreciable cholesteryl ester (CE) accumulation in cultured macrophages (J774A.1). In the present study, we examined whether oxidation of type III HTG-VLDL would enhance their uptake by J774A.1 cells. Type III HTG-VLDL were oxidized as measured by both conjugated-diene formation and increased electrophoretic mobility on agarose gels. Both LDL and type III HTG-VLDL undergo oxidation, albeit under different kinetic parameters. From the conjugated-diene curve, type III HTG-VLDL, compared with LDL, were found to have a 6-fold longer lag time, to take 6-fold longer to reach maximal diene production, and to produce a 2-fold greater amount of dienes but at half the rate (all P <.005). Incubation of macrophages with either native type III HTG-VLDL or LDL (50 μg lipoprotein cholesterol/mL media for 16 hours) caused small increases (4-fold and 2.7-fold, respectively) in cellular CE levels relative to control cells (both P =.0001). After 24 hours of CuSO 4 exposure, we found that oxidized type III HTG-VLDL and LDL caused a 9.4-fold and 10.5-fold increase, respectively, in cellular CE levels ( P =.0001). We next examined whether extending the exposure period for type III HTG-VLDL to CuSO 4 beyond 24 hours would further enhance its ability to induce macrophage CE accumulation. After 48 hours of CuSO 4 exposure, type III HTG-VLDL and LDL caused 21.3-fold and 11.6-fold increases, respectively, in cellular CE levels ( P =.0001). The cellular CE loading achieved with 48 hour–oxidized type III HTG-VLDL was significantly higher than either 24 hour–oxidized type III HTG-VLDL (2.3-fold, P =.003) or 48 hour–oxidized LDL (1.8-fold, P =.012). There was no significant difference between the CE loading achieved by incubation of cells with either 24 hour–oxidized type III HTG-VLDL, 24 hour–oxidized LDL, or 48 hour–oxidized LDL ( P ≥.518). In this study, we also examined whether partial lipolysis (19% to 50% triglyceride hydrolysis) of type III HTG-VLDL to produce remnants would increase the susceptibility of the lipoprotein to oxidative modification and subsequent cellular CE loading. Forty-eight hour–oxidized type III VLDL-remnants stimulated CE accumulation 30.4-fold over baseline ( P =.0001). In contrast, nonoxidized type III VLDL-remnants caused the same very low level of CE loading as did native type III HTG-VLDL ( P =.680). The increase in cellular CE levels achieved with 48 hour–oxidized type III VLDL-remnants was significantly higher than that achieved with 48 hour–oxidized type III HTG-VLDL ( P =.047). In conclusion, we have shown that oxidized type III HTG-VLDL will induce macrophage CE accumulation well above levels achieved with oxidized LDL. In addition, we also showed that by forming a VLDL-remnant before oxidative modification, we can further enhance macrophage CE accumulation. These results provide a potential mechanism for the atherogenicity of type III HTG-VLDL and their remnants.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Integrity signals

Registry

Crossref · 10.1161/01.atv.17.9.1707

Cites

63 of 63 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Macrophage uptake of remnant particles in native or modified forms elicits an inflammatory response, thereby promoting atherosclerosis.
“Macrophage uptake of remnant particles in native or modified forms elicits an inflammatory response, thereby promoting atherosclerosis.151,152”
From Triglyceride-rich lipoproteins and their remnants: metabolic insights, role in atherosclerotic cardiovascular disease, and emerging therapeutic strategies—a consensus statement from the European Atherosclerosis Society (2021) · cites this paper as [152]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

The Metabolic Basis of Inherited Disease.
(1988) · Annals of Internal Medicine · doi:10.7326/0003-4819-108-3-503_7 · Cited by 7,807 · see citing works
A modification of the Lowry procedure to simplify protein determination in membrane and lipoprotein samples
Markwell, M. A. K., Haas, S. M., BIEBER, L. L., & Tolbert, N. E. (1978) · Analytical Biochemistry · doi:10.1016/0003-2697(78)90586-9 · Cited by 6,460 · see citing works
Beyond Cholesterol
Epstein, F. H., Steinberg, D. I., Parthasarathy, S., Carew, T. E., Khoo, J. C., & Witztum, J. L. (1989) · New England Journal of Medicine · doi:10.1056/nejm198904063201407 · Cited by 6,425 · see citing works
Apolipoprotein E: Cholesterol Transport Protein with Expanding Role in Cell Biology
Mahley, R. W. (1988) · Science · doi:10.1126/science.3283935 · Cited by 4,028 · see citing works
Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with HhaI.
Hixson, J., & Vernier, D. (1990) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)43176-1 · Cited by 2,933 · see citing works
Role of oxidized low density lipoprotein in atherogenesis.
Witztum, J. L., & Steinberg, D. H. (1991) · Journal of Clinical Investigation · doi:10.1172/jci115499 · Cited by 2,682 · see citing works
Binding site on macrophages that mediates uptake and degradation of acetylated low density lipoprotein, producing massive cholesterol deposition
Goldstein, J. L., Ho, Y. K., Basu, S. K., & Brown, M. S. (1979) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.76.1.333 · Cited by 2,447 · see citing works
The role of lipid peroxidation and antioxidants in oxidative modification of LDL
Esterbauer, H., Gebicki, J. M., Puhl, H., & Jürgens, G. (1992) · Free Radical Biology and Medicine · doi:10.1016/0891-5849(92)90181-f · Cited by 2,307 · see citing works
LIPOPROTEIN METABOLISM IN THE MACROPHAGE: Implications for Cholesterol Deposition in Atherosclerosis
Brown, M. S., & Goldstein, J. L. (1983) · Annual Review of Biochemistry · doi:10.1146/annurev.bi.52.070183.001255 · Cited by 2,300 · see citing works
Severe hypercholesterolemia and atherosclerosis in apolipoprotein E-deficient mice created by homologous recombination in ES cells
Plump, A. S., Smith, J. D., Hayek, T., Aalto-Setälä, K., Walsh, A., Verstuyft, J. G., Rubin, E. M., & Breslow, J. L. (1992) · Cell · doi:10.1016/0092-8674(92)90362-g · Cited by 2,263 · see citing works
ApoE-deficient mice develop lesions of all phases of atherosclerosis throughout the arterial tree.
Nakashima, Y., Plump, A. S., Raines, E. W., Breslow, J. L., & Ross, R. (1994) · Arteriosclerosis and Thrombosis: A Journal of Vascular Biology · doi:10.1161/01.atv.14.1.133 · Cited by 1,693 · see citing works
Modification of low density lipoprotein by endothelial cells involves lipid peroxidation and degradation of low density lipoprotein phospholipids.
Steinbrecher, U. P., Parthasarathy, S., Leake, D. S., Witztum, J. L., & Steinberg, D. I. (1984) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.81.12.3883 · Cited by 1,626 · see citing works
The role of the monocyte in atherogenesis: I. Transition of blood-borne monocytes into foam cells in fatty lesions.
Rg, G. (1981) · PubMed · Cited by 1,317 · see citing works
Enhanced macrophage degradation of low density lipoprotein previously incubated with cultured endothelial cells: recognition by receptors for acetylated low density lipoproteins.
Henriksen, T., Mahoney, E. M., & Steinberg, D. H. (1981) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.78.10.6499 · Cited by 1,024 · see citing works
Malondialdehyde alteration of low density lipoproteins leads to cholesteryl ester accumulation in human monocyte-macrophages
Fogelman, A. M., Shechter, I., Seager, J., Hokom, M. M., CHILD, J. S., & Edwards, P. A. (1980) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.77.4.2214 · Cited by 849 · see citing works
Atherosclerosis in mice lacking apo E. Evaluation of lesional development and progression
Reddick, R. L., Zhang, S. H., & Maeda, N. (1994) · Arteriosclerosis and Thrombosis: A Journal of Vascular Biology · doi:10.1161/01.atv.14.1.141 · Cited by 633 · see citing works
Biochemical structural and functional properties of oxidized low-density lipoprotein
Esterbauer, H., Dieber‐Rotheneder, M., Waeg, G., Striegl, G., & Juergens, G. (1990) · Chemical Research in Toxicology · doi:10.1021/tx00014a001 · Cited by 534 · see citing works
ApoE-deficient mice are a model of lipoprotein oxidation in atherogenesis. Demonstration of oxidation-specific epitopes in lesions and high titers of autoantibodies to malondialdehyde-lysine in serum.
Palinski, W., Ord, V. A., Plump, A. S., Breslow, J. L., Steinberg, D. H., & Witztum, J. L. (1994) · Arteriosclerosis and Thrombosis A Journal of Vascular Biology · doi:10.1161/01.atv.14.4.605 · Cited by 488 · see citing works
Prevention of atherosclerosis in apolipoprotein E-deficient mice by bone marrow transplantation
Linton, M. F., Atkinson, J. B., & Fazio, S. (1995) · Science · doi:10.1126/science.7863332 · Cited by 478 · see citing works
Arterial foam cells with distinctive immunomorphologic and histochemical features of macrophages.
Schaffner, T., Taylor, K., Bartucci, E. J., Fischer-Dzoga, K., Beeson, J. H., Glagov, S. K., & Wissler, R. W. (1980) · PubMed Central · Cited by 475 · see citing works
Decrease in reactive amino groups during oxidation or endothelial cell modification of LDL. Correlation with changes in receptor-mediated catabolism.
Steinbrecher, U. P., Witztum, J. L., Parthasarathy, S., & Steinberg, D. H. (1987) · Arteriosclerosis An Official Journal of the American Heart Association Inc · doi:10.1161/01.atv.7.2.135 · Cited by 468 · see citing works
Apolipoprotein E alleles, dyslipidemia, and coronary heart disease. The Framingham Offspring Study
Wilson, P. W. F. (1994) · JAMA · doi:10.1001/jama.1994.03520210050031 · Cited by 468 · see citing works
Improved Measurement of Low-Density-Lipoprotein Susceptibility to Copper-Induced Oxidation: Application of a Short Procedure for Isolating Low-Density Lipoprotein
Kleinveld, H. A., Hak-Lemmers, H. L. M., Stalenhoef, A. F. H., & Demacker, P. N. M. (1992) · Clinical Chemistry · doi:10.1093/clinchem/38.10.2066 · Cited by 348 · see citing works
Effect of Antioxidants on Oxidative Modification of LDL
Esterbauer, H., Puhl, H., Dieber‐Rotheneder, M., Waeg, G., & Rabl, H. (1991) · Annals of Medicine · doi:10.3109/07853899109150520 · Cited by 261 · see citing works
Modification of human low-density lipoprotein by the lipid peroxidation product 4-hydroxynonenal
Jürgens, G., Lång, J., & Esterbauer, H. (1986) · Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism · doi:10.1016/0005-2760(86)90016-0 · Cited by 237 · see citing works
Pathogenesis and Management of Lipoprotein Disorders
Flier, J. S., Underhill, L. H., Schaefer, E. J., & Levy, R. I. (1985) · New England Journal of Medicine · doi:10.1056/nejm198505163122007 · Cited by 213 · see citing works
Hypertriglyceridemic Very Low Density Lipoproteins Induce Triglyceride Synthesis and Accumulation in Mouse Peritoneal Macrophages
Gianturco, S. H., Bradley, W. A., Gotto, A. M., Morrisett, J. D., & Peavy, D. L. (1982) · Journal of Clinical Investigation · doi:10.1172/jci110590 · Cited by 199 · see citing works
INTERACTION BETWEEN OLEATE AND THE LIPOPROTEINS OF HUMAN SERUM
Gordon, R. S. (1955) · Journal of Clinical Investigation · doi:10.1172/jci103097 · Cited by 197 · see citing works
Pathogenesis and Management of Lipoprotein Disorders
Fredman, S. (1986) · New England Journal of Medicine · doi:10.1056/nejm198603273141310 · Cited by 187 · see citing works
Apolipoprotein E phenotyping with a single gel method: application to the study of informative matings.
Bouthillier, D., Sing, C. F., & Davignon, J. (1983) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)37920-7 · Cited by 176 · see citing works
Increased Plasma and Lipoprotein Lipid Peroxidation in apo E-Deficient Mice
Hayek, T., Oiknine, J., Brook, J. G., & Aviram, M. (1994) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1994.1883 · Cited by 171 · see citing works
Obligatory role of cholesterol and apolipoprotein E in the formation of large cholesterol-enriched and receptor-active high density lipoproteins.
Koo, C., Innerarity, T. L., & Mahley, R. W. (1985) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)38968-8 · Cited by 162 · see citing works
Enhanced in vitro oxidation of plasma lipoproteins derived from hypercholesterolemic patients
Lavy, A., Brook, G. J., Dankner, G., Amotz, A. B., & Aviram, M. (1991) · Metabolism · doi:10.1016/0026-0495(91)90005-h · Cited by 156 · see citing works
Structural and metabolic heterogeneity of beta-very low density lipoproteins from cholesterol-fed dogs and from humans with type III hyperlipoproteinemia.
Fainaru, M., Mahley, R. W., Hamilton, R. L., & Innerarity, T. L. (1982) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)38102-5 · Cited by 156 · see citing works
The role of lipoprotein lipase in the metabolism of triglyceride-rich lipoproteins by macrophages.
Lindqvist, P., Östlund‐Lindqvist, A., Witztum, J. L., Steinberg, D. H., & Little, J. A. (1983) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)44634-5 · Cited by 148 · see citing works
Improved Method for Determination of Triglycerides in Serum
Neri, B. P., & Frings, C. S. (1973) · Clinical Chemistry · doi:10.1093/clinchem/19.10.1201 · Cited by 146 · see citing works
Oxidative modification of beta-very low density lipoprotein. Potential role in monocyte recruitment and foam cell formation.
Parthasarathy, S., Quinn, M. T., Schwenke, D. C., Carew, T. E., & Steinberg, D. H. (1989) · Arteriosclerosis An Official Journal of the American Heart Association Inc · doi:10.1161/01.atv.9.3.398 · Cited by 145 · see citing works
Genetic Basis of Lipoprotein Disorders
Dammerman, M., & Breslow, J. L. (1995) · Circulation · doi:10.1161/01.cir.91.2.505 · Cited by 110 · see citing works
Apolipoprotein E is the determinant that mediates the receptor uptake of beta-very low density lipoproteins by mouse macrophages.
Innerarity, T. L., Arnold, K. S., Weisgraber, K. H., & Mahley, R. W. (1986) · Arteriosclerosis An Official Journal of the American Heart Association Inc · doi:10.1161/01.atv.6.1.114 · Cited by 87 · see citing works
Detection of new epitopes formed upon oxidation of low-density lipoprotein, lipoprotein (a) and very-low-density lipoprotein. Use of an antiserum against 4-hydroxynonenal-modified low-density lipoprotein
Jürgens, G., Ashy, A., & Esterbauer, H. (1990) · Biochemical Journal · doi:10.1042/bj2650605 · Cited by 81 · see citing works
Onset of apoprotein E secretion during differentiation of mouse bone marrow-derived mononuclear phagocytes.
Werb, Z., & Chin, J. R. (1983) · The Journal of Cell Biology · doi:10.1083/jcb.97.4.1113 · Cited by 79 · see citing works
Apolipoprotein E and lipoprotein lipase secreted from human monocyte-derived macrophages modulate very low density lipoprotein uptake.
Ishibashi, S., Yamada, N., Shimano, H., Mori, N., Mokuno, H., Gotohda, T., Kawakami, M., Murase, T., & Takaku, F. (1990) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(19)39730-3 · Cited by 78 · see citing works
Cholesterol accumulation in J774 macrophages induced by triglyceride-rich lipoproteins. Comparison of very low density lipoprotein from subjects with type III, IV, and V hyperlipoproteinemias.
Huff, M. W., Evans, A. J., Sawyez, C. G., Wolfe, B. M. J., & Nestel, P. J. (1991) · Arteriosclerosis and Thrombosis A Journal of Vascular Biology · doi:10.1161/01.atv.11.2.221 · Cited by 74 · see citing works
Self-citation
Lipoprotein modification
Chait, A., & Heinecke, J. W. (1994) · Current Opinion in Lipidology · doi:10.1097/00041433-199410000-00008 · Cited by 73 · see citing works
Evidence that cholesteryl ester and triglyceride accumulation in J774 macrophages induced by very low density lipoprotein subfractions occurs by different mechanisms
Evans, A. J., Sawyez, C. G., Wolfe, B. M. J., Connelly, P. W., Maguire, G., & Huff, M. (1993) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)39692-9 · Cited by 61 · see citing works
Self-citation
Radical-mediated oxidation of isolated human very-low-density lipoprotein.
Mohr, D., & Stocker, R. (1994) · Arteriosclerosis and Thrombosis A Journal of Vascular Biology · doi:10.1161/01.atv.14.7.1186 · Cited by 57 · see citing works
Monoclonal antibodies to bovine milk lipoprotein lipase. Evidence for proteolytic degradation of the native enzyme.
Socorro, L., & Jackson, R. L. (1985) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)88974-8 · Cited by 48 · see citing works
Lipolysis is a prerequisite for lipid accumulation in HepG2 cells induced by large hypertriglyceridemic very low density lipoproteins.
Evans, A. J., Sawyez, C. G., Wolfe, B. M. J., & Huff, M. W. (1992) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(19)50081-3 · Cited by 41 · see citing works
Self-citation
Lipolysis-induced partitioning of free fatty acids to lipoproteins: effect on the biological properties of free fatty acids.
Chung, B. H., Tallis, G. A., Cho, B. H., Segrest, J. P., & Henkin, Y. (1995) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)41114-9 · Cited by 40 · see citing works
Apoprotein E mediates the interaction of beta-VLDL with macrophages.
Bates, S. R., Coughlin, B. A., Mazzone, T., Borensztajn, J., & Getz, G. S. (1987) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)38647-8 · Cited by 39 · see citing works
EFFECTS OF HEPARIN ON THE LIPOPROTEINS IN HYPERLIPEMIA. AN ELECTROPHORETIC STUDY OF THE SERUM ALPHA AND BETA LIPOPROTEINS AFTER THEIR SEPARATION BY FRACTIONATION OF THE PLASMA PROTEINS OR ULTRACENTRIFUGAL FLOTATION 1
Herbst, F. S. M., Lever, W. F., Lyons, M. E., & Hurley, N. A. (1955) · Journal of Clinical Investigation · doi:10.1172/jci103106 · Cited by 37 · see citing works
Oxidation of LDL: Role in atherogenesis
Hoff, H. F., & O'NEIL, J. A. (1991) · Journal of Molecular Medicine · doi:10.1007/bf01645153 · Cited by 35 · see citing works
Accumulation of an apoE-poor subfraction of very low density lipoprotein in hypertriglyceridemic men.
Evans, A. J., Huff, M. W., & Wolfe, B. M. J. (1989) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)38218-3 · Cited by 31 · see citing works
Self-citation
Oxidation of beta-very low density lipoprotein by endothelial cells enhances its metabolism by smooth muscle cells in culture.
Horrigan, S., Campbell, J. H., & CAMPBELL, G. R. (1991) · Arteriosclerosis and Thrombosis A Journal of Vascular Biology · doi:10.1161/01.atv.11.2.279 · Cited by 28 · see citing works
Apolipoprotein E and lipoprotein lipase reduce macrophage degradation of oxidized very-low-density lipoprotein (VLDL), but increase cellular degradation of native VLDL
Keidar, S., Kaplan, M., Rosenblat, M., Brook, G. J., & Aviram, M. (1992) · Metabolism · doi:10.1016/0026-0495(92)90007-w · Cited by 24 · see citing works
Metabolism of apolipoproteins C-II, C-III, and B in hypertriglyceridemic men. Changes after heparin-induced lipolysis.
Huff, M. W., Breckenridge, W. C., Strong, W., & Wolfe, B. M. J. (1988) · Arteriosclerosis An Official Journal of the American Heart Association Inc · doi:10.1161/01.atv.8.5.471 · Cited by 22 · see citing works
Self-citation
Very low density lipoproteins stimulate cholesteryl ester formation in U937 macrophages. Heterogeneity and biologic variation among normal humans.
Sacks, F. M., & Breslow, J. L. (1987) · Arteriosclerosis An Official Journal of the American Heart Association Inc · doi:10.1161/01.atv.7.1.35 · Cited by 22 · see citing works
NMR Analysis of Low-Density Lipoprotein Oxidatively-Modifiedin vztro
Barenghi, L., Bradamante, S., Giudici, G. A., & Verganl, C. (1990) · Free Radical Research Communications · doi:10.3109/10715769009087991 · Cited by 22 · see citing works
Preferential metabolism by macrophages of conditioned rabbit hypercholesterolemic remnant lipoproteins
Haratz, D., Stein, O. T., Shwartz, R., Berry, E. M., & Stein, Y. (1988) · Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism · doi:10.1016/0005-2760(88)90023-9 · Cited by 21 · see citing works
Recognition sites on rat liver cells for oxidatively modified beta-very low density lipoproteins.
de Rijke, Y. B., HESSELS, E. M. A. J., & van Berkel, T. J. (1992) · Arteriosclerosis and Thrombosis A Journal of Vascular Biology · doi:10.1161/01.atv.12.1.41 · Cited by 20 · see citing works
Identification and metabolic characteristics of an apolipoprotein C-II variant isolated from a hypertriglyceridemic subject.
Huff, M. W., Evans, A., Wolfe, B. M. J., Connelly, P. W., Maguire, G., & Strong, W. (1990) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)43161-x · Cited by 13 · see citing works
Self-citation
Very-Low-Density and Low-Density Lipoproteins Induce Nitric Oxide Synthesis in Macrophages
Mohan, P. F., & Desaiah, D. (1994) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1994.2568 · Cited by 11 · see citing works
ApoE-3-specific metabolism of human plasma very low density lipoproteins in cultured J-774 macrophages.
Granot, E., & Eisenberg, S. (1990) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)42099-1 · Cited by 10 · see citing works

Flagged first, then by citations

Research works printed but not linked: 6

Huflf MW, Evans AJ, Sawyez CG, Wolfe BM, Nestel PJ. Choles- terol accumulation in J774 macrophages induced by triglycer- ide-rich lipoproteins: a comparison of VLDL from subjects with types III, IV, and V hyperlipoproteinemia. Arterioscler Thromb. 1991;11:221-233.
Gianturco SH, Bradley WA, Gotto AM, Morrisett JD, Peavy DL. Hypertriglyceridemic very low density lipoproteins induce triglyc- eride synthesis in mouse peritoneal macrophages. J Clin Invest. 1982;70:168-178.
Socorro L, Jackson RL. Monoclonal antibodies to bovine milk lipoprotein lipase. J Biol Chem. 1985;260:6324-6328.
Steinbrecher UP, Witztum JL, Parthasarathy S, Steinberg D. Decrease in reactive amino groups during oxidation or endothelial cell modification of LDL. Arteriosclerosis. 1987;7:135-143.
Barenghi L, Bradamante S, Giudici GA, Vergani C. NMR analysis of low-density lipoprotein oxidatively-modified in vitro. Free Radio Res Commun. 1990;8:175-183.
Jurgens G, Ashy A, Esterbauer H. Detection of new epitopes formed upon oxidation of low density lipoprotein, lipoprotein (a) and very low density lipoprotein. Biochem J. 1990;265:605-608.

Sorted by citations

Triglyceride-rich lipoproteins and their remnants: metabolic insights, role in atherosclerotic cardiovascular disease, and emerging therapeutic strategies—a consensus statement from the European Atherosclerosis Society
Ginsberg, H. N., Packard, C. J., Chapman, M. J., Borén, J., Aguilar-Salinas, C. A., Averna, M., Ference, B. A., Gaudet, D., Hegele, R. A., Kersten, S., et al. (2021) · European Heart Journal · doi:10.1093/eurheartj/ehab551 · Cited by 979 · see citing works
“151,152 • Emerging pathophysiological and metabolic evidence supports the putative atherogenicity of apoB48-and apoB100-containing remnants during the postprandial period, with apoB100-containing particles predominating. composition after dietary fat absorption.”
BackgroundSelf-citation
Remnants of the triglyceride-rich lipoproteins, diabetes, and cardiovascular disease
Chait, A., Ginsberg, H. N., Vaisar, T., Heinecke, J. W., Goldberg, I. J., & Bornfeldt, K. E. (2020) · Diabetes · doi:10.2337/dbi19-0007 · Cited by 229 · see citing works
“In contrast to unmodified LDL, native RLPs promote rapid cholesterol accumulation by macrophages (52,53), suggesting that RLPs are much more potent on a per particle basis than LDL at producing macrophage foam cells in vivo.”
Background
Multifunctional roles of macrophages in the development and progression of atherosclerosis in humans and experimental animals
Takahashi, K. I., Takeya, M., & Sakashita, N. (2002) · Medical Molecular Morphology · doi:10.1007/s007950200023 · Cited by 192 · see citing works
“-VLDL is taken up by macrophages in vitro during incubation at 37°C, and this uptake is enhanced by oxidation after remnant formation.(115) Candidates for receptors recognizing -VLDL are VLDL receptor (VLDLR), LDLR, and LDLR-related protein (LRP).”
Background
Detection, quantification, and characterization of potentially atherogenic triglyceride-rich remnant lipoproteins
Cohn, J. S., Marcoux, C., & Davignon, J. (1999) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/01.atv.19.10.2474 · Cited by 156 · see citing works
Regulation of Macrophage Cholesterol Efflux through Hydroxymethylglutaryl-CoA Reductase Inhibition
Argmann, C., Edwards, J. Y., Sawyez, C. G., O’Neil, C. H., Hegele, R. A., Pickering, J. G., & Huff, M. W. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m502761200 · Cited by 129 · see citing works
Self-citation
Selective Up-regulation of LXR-regulated Genes ABCA1, ABCG1, and APOE in Macrophages through Increased Endogenous Synthesis of 24(S),25-Epoxycholesterol
Beyea, M. M., Heslop, C., Sawyez, C. G., Edwards, J. Y., Markle, J., Hegele, R. A., & Huff, M. W. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.m611063200 · Cited by 104 · see citing works
Self-citation
Hyperlipoproteinemia Type 3: The Forgotten Phenotype
Hopkins, P. N., Brinton, E. A., & Nanjee, M. N. (2014) · Current Atherosclerosis Reports · doi:10.1007/s11883-014-0440-2 · Cited by 88 · see citing works
Transforming Growth Factor-β1 Inhibits Macrophage Cholesteryl Ester Accumulation Induced by Native and Oxidized VLDL Remnants
Argmann, C., Diepstraten, C. V. D., Sawyez, C. G., Edwards, J. Y., Hegele, R. A., Wolfe, B. M. J., & Huff, M. W. (2001) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/hq1201.099426 · Cited by 81 · see citing works
Self-citation
Monocytes and macrophages as protagonists in vascular complications of diabetes
Kanter, J. E., Hsu, C.-C., & Bornfeldt, K. E. (2020) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2020.00010 · Cited by 76 · see citing works
Modification of lipoprotein metabolism and function driving atherogenesis in diabetes
Luciani, L., Pedrelli, M., & Parini, P. (2024) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2024.117545 · Cited by 72 · see citing works
Improvement of endothelial vasomotor dysfunction by treatment with alpha-tocopherol in patients with high remnant lipoproteins levels
Kugiyama, K., Motoyama, T., Doi, H., Kawano, H., Hirai, N., Soejima, H., Miyao, Y., Takazoe, K., Moriyama, Y., Mizuno, Y., et al. (1999) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(99)00057-1 · Cited by 70 · see citing works
“It has recently been reported that oxidatively modified remnant lipoproteins caused greater formation of foam cells in in vitro experiments than native remnant lipoproteins (22), suggesting that oxidized remnant lipoproteins may also play an important role in atherogenesis in hyperlipidemic patients.”
Background
Hypotensive, Hypolipidemic, and Vascular Protective Effects of Morus alba L. in Rats Fed an Atherogenic Diet
Lee, Y. J., Choi, D. H., Kim, E. J., Kim, H. Y., Kwon, T. O., Kang, D. G., & Lee, H. S. (2011) · The American Journal of Chinese Medicine · doi:10.1142/s0192415x11008634 · Cited by 68 · see citing works
All ApoB-Containing Lipoproteins Induce Monocyte Chemotaxis and Adhesion When Minimally Modified
Lee, C., Sigari, F., Segrado, T., Hörkkö, S., Hama, S. Y., Subbaiah, P. V., Miwa, M., Navab, M., Witztum, J. L., & Reaven, P. D. (1999) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.19.6.1437 · Cited by 63 · see citing works
APOA5 genetic variants are markers for classic hyperlipoproteinemia phenotypes and hypertriglyceridemia
Wang, J., Ban, M. R., Kennedy, B. A., Anand, S. S., Yusuf, S., Huff, M. W., Pollex, R. L., & Hegele, R. A. (2008) · Nature Clinical Practice Cardiovascular Medicine · doi:10.1038/ncpcardio1326 · Cited by 62 · see citing works
Self-citation
Hypertriglyceridemia and Atherosclerosis: Using Human Research to Guide Mechanistic Studies in Animal Models
Basu, D., & Bornfeldt, K. (2020) · Frontiers in Endocrinology · doi:10.3389/fendo.2020.00504 · Cited by 51 · see citing works
“Once in the subendothelial space, RLPs are trapped by proteoglycans (18, 29) and can be taken up by lesional macrophages (30, 31).”
Background
Human Smooth Muscle Cell Subpopulations Differentially Accumulate Cholesteryl Ester When Exposed to Native and Oxidized Lipoproteins
Argmann, C., Sawyez, C. G., Li, S., Nong, Z., Hegele, R. A., Pickering, J. G., & Huff, M. W. (2004) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000131260.80316.37 · Cited by 48 · see citing works
Self-citation
Cumulative exposure to high remnant-cholesterol concentrations increases the risk of cardiovascular disease in patients with hypertension: a prospective cohort study
Wu, W., Chen, G., Wu, K., Zheng, H., Chen, Y., Wang, X., Huang, Z., Cai, Z., Cai, Z., Chen, Z., et al. (2023) · Cardiovascular Diabetology · doi:10.1186/s12933-023-01984-4 · Cited by 43 · see citing works
“A combination of abnormal RC and hypertension may promote atherosclerosis, impaired arterial compliance, vascular endothelial dysfunction, chronic inflammatory responses, and vascular remodeling, which are involved in the pathogenesis of CVD [40, 42, 43, 46].”
Background
Elevated Uric Acid Levels Promote Vascular Smooth Muscle Cells (VSMC) Proliferation via an Nod-Like Receptor Protein 3 (NLRP3)-Inflammasome-Dependent Mechanism
Li, H., Qian, F., Liu, H., & Zhang, Z. (2019) · Medical Science Monitor · doi:10.12659/msm.916667 · Cited by 43 · see citing works
“[29] found that allopurinol could protect endothelial cell function in patients with coronary heart disease.”
Background
Arctium lappa ameliorates endothelial dysfunction in rats fed with high fat/cholesterol diets
Lee, Y. J., Choi, D. H., Cho, G.-H., Kim, J. S., Kang, D. G., & Lee, H. S. (2012) · BMC Complementary and Alternative Medicine · doi:10.1186/1472-6882-12-116 · Cited by 40 · see citing works
“Elevated LDLcholesterol levels impair endothelial function, and LDLcholesterol deposited in blood vessel wall forms part of the atherosclerotic plaque [28,29].”
Background
The iterative lipid impact on inflammation in atherosclerosis
Kraaijenhof, J. M., Hovingh, G. K., Stroes, E. S. G., & Kroon, J. (2021) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000779 · Cited by 39 · see citing works
“Apart from receptor mediated uptake, TRLs may also be taken up by macrophages in a receptorindependent manner suggesting a potent ability of TRLs in enhancing foam cell formation [51,52].”
Background
The Atherogenic Significance of an Elevated Plasma Triglyceride Level
Ooi, T. C., & Ooi, D. S. (1998) · Critical Reviews in Clinical Laboratory Sciences · doi:10.1080/10408369891234255 · Cited by 37 · see citing works
GENETICS OF LIPOPROTEIN DISORDERS
Davignon, J., & Genest, J. J. (1998) · Endocrinology and Metabolism Clinics of North America · doi:10.1016/s0889-8529(05)70024-4 · Cited by 37 · see citing works
Eicosapentaenoic Acid Improves Endothelial Function in Hypertriglyceridemic Subjects Despite Increased Lipid Oxidizability
Okumura, T., Fujioka, Y., Morimoto, S., Tsuboi, S., Masai, M., Tsujino, T., Ohyanagi, M., & Iwasaki, T. (2002) · The American Journal of the Medical Sciences · doi:10.1097/00000441-200211000-00003 · Cited by 36 · see citing works
Identification of lipid binding and lipoprotein lipase activation domains of human apoAV
Sun, G., Bi, N., Li, G., Zhu, X., Zeng, W., Wu, G., Xue, H., & Chen, B. (2006) · Chemistry and Physics of Lipids · doi:10.1016/j.chemphyslip.2006.04.004 · Cited by 35 · see citing works
History and future of omega-3 fatty acids in cardiovascular disease
Sperling, L. S., & Nelson, J. R. (2016) · Current Medical Research and Opinion · doi:10.1185/03007995.2015.1120190 · Cited by 34 · see citing works
Preferential reduction of very low density lipoprotein-1 particle number by fenofibrate in type IIB hyperlipidemia: consequences for lipid accumulation in human monocyte-derived macrophages
Milosavljevic, D., Griglio, S., Naour, G. L., & Chapman, M. J. (2001) · Atherosclerosis · doi:10.1016/s0021-9150(00)00634-1 · Cited by 34 · see citing works
Hypertriglyceridemia: A Review of Clinical Relevance and Treatment Options: Focus on Cerivastatin
Breuer, H.-W. M. (2001) · Current Medical Research and Opinion · doi:10.1185/03007990152005379 · Cited by 31 · see citing works
Oxidized VLDL Induces Less Triglyceride Accumulation in J774 Macrophages Than Native VLDL Due to an Impaired Extracellular Lipolysis
Jong, M. C., Hendriks, W. L., van Vark, L. C., Dahlmans, V. E. H., Groener, J. E. M., & Havekes, L. M. (2000) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.20.1.144 · Cited by 30 · see citing works
Effect of meals rich in heated olive and safflower oils on oxidation of postprandial serum in healthy men
Sutherland, W. H. F., de Jong, S. A., Walker, R. J., Williams, M. J. A., Skeaff, C. M., Duncan, A. W., & Harper, M. J. (2002) · Atherosclerosis · doi:10.1016/s0021-9150(01)00561-5 · Cited by 29 · see citing works
“Both oxidised TGRLP remnant particles [37,38] and oxidised LDL are potentially atherogenic.”
Background
Modification of Type III VLDL, Their Remnants, and VLDL From ApoE-Knockout Mice by p -Hydroxyphenylacetaldehyde, a Product of Myeloperoxidase Activity, Causes Marked Cholesteryl Ester Accumulation in Macrophages
Whitman, S. C., Hazen, S. L., Miller, D. B., Hegele, R. A., Heinecke, J. W., & Huff, M. W. (1999) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.19.5.1238 · Cited by 28 · see citing works
Self-citation
The Oxysterol 24 (S) ,25‐Epoxycholesterol Attenuates Human Smooth Muscle–Derived Foam Cell Formation Via Reduced Low‐Density Lipoprotein Uptake and Enhanced Cholesterol Efflux
Beyea, M. M., Reaume, S., Sawyez, C. G., Edwards, J. Y., O’Neil, C. H., Hegele, R. A., Pickering, J. G., & Huff, M. W. (2012) · Journal of the American Heart Association · doi:10.1161/jaha.112.000810 · Cited by 27 · see citing works
Self-citation
Casein and Soy Protein Isolate in Experimental Atherosclerosis: Influence on Hyperlipidemia and Lipoprotein Oxidation
Damasceno, N. R. T., Gidlund, M., Goto, H., Dias, C. T. D. S., Okawabata, F. S., & Abdalla, D. S. P. (2001) · Annals of Nutrition and Metabolism · doi:10.1159/000046704 · Cited by 27 · see citing works
The role of systemic inflammation in remnant cholesterol-associated cardiovascular risk: insights from the EPIC-Norfolk study
Kraaijenhof, J. M., Kerkvliet, M., Nurmohamed, N. S., Grefhorst, A., Kroon, J., Wareham, N. J., Hovingh, G. K., Stroes, E. S. G., Boekholdt, S. M., & Reeskamp, L. F. (2025) · European Journal of Preventive Cardiology · doi:10.1093/eurjpc/zwaf037 · Cited by 27 · see citing works
Improved Endothelial Dysfunction by Cynanchum wilfordii in Apolipoprotein E −/− Mice Fed a High Fat/Cholesterol Diet
Choi, D. H., Lee, Y. J., Oh, H. C., Cui, Y., Kim, J. S., Kang, D. G., & Lee, H. S. (2011) · Journal of Medicinal Food · doi:10.1089/jmf.2010.1222 · Cited by 24 · see citing works
“Elevated total and LDLcholesterol levels impair endothelial function, and LDLcholesterol is deposited in the blood vessel wall as part of atherosclerotic plaques.(22,23) However, increased HDLcholesterol could suppress the atherosclerotic process by facilitating translocation of cholesterol from peripheral tissues lik…”
Background
The Remnant Lipoprotein Hypothesis of Diabetes-Associated Cardiovascular Disease
Bornfeldt, K. (2022) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.122.317163 · Cited by 22 · see citing works
Association between remnant cholesterol, metabolic syndrome, and cardiovascular disease: post hoc analysis of a prospective national cohort study
Jin, J., Hu, X., François, M., Zeng, P., Wang, W., Yu, B., Zhou, Y., & Dong, H. (2023) · European journal of medical research · doi:10.1186/s40001-023-01369-z · Cited by 22 · see citing works
“Furthermore, it is difficult for RC to diffuse back to blood stream, since RC has larger scales compared to LDL-C [45, 46].”
Background
Uptake of type IV hypertriglyceridemic VLDL by cultured macrophages is enhanced by interferon-γ
Whitman, S. C., Argmann, C., Sawyez, C. G., Miller, D. B., Hegele, R. A., & Huff, M. W. (1999) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)33505-7 · Cited by 21 · see citing works
Self-citation
The LDL receptor is the major pathway for β-VLDL uptake by mouse peritoneal macrophages
Perrey, S., Ishibashi, S., Kitamine, T., Osuga, J.-I., Yagyu, H., Chen, Z., Shionoiri, F., Iizuka, Y., Yahagi, N., Tamura, Y., et al. (2001) · Atherosclerosis · doi:10.1016/s0021-9150(00)00457-3 · Cited by 21 · see citing works
Plasma metabolism of apoB-containing lipoproteins in patients with hepatic lipase deficiency
Ruel, I. L., Couture, P., Cohn, J. S., & Lamarche, B. (2005) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2004.12.014 · Cited by 21 · see citing works
2019 George Lyman Duff Memorial Lecture
Hegele, R., & Dron, J. (2020) · Arteriosclerosis, Thrombosis and Vascular Biology · doi:10.1161/atvbaha.120.313065 · Cited by 14 · see citing works
Self-citation
Remnant Cholesterol
Bruemmer, D., & Cho, L. (2021) · Circulation Cardiovascular Imaging · doi:10.1161/circimaging.121.012615 · Cited by 18 · see citing works
Type III hyperlipoproteinema with apolipoprotein E2/2 genotype in Japan
Eto, M., Saito, M., Nakata, H., Iwashima, Y., Watanabe, K., Ikoda, A., & Kaku, K. (2002) · Clinical Genetics · doi:10.1034/j.1399-0004.2002.610604.x · Cited by 16 · see citing works
“There is a possibility that remnant lipoproteins from diabetic type III HLP patients may undergo glycation and further oxidation (31,32) and therefore may be avidly taken up by macrophages, causing massive accumulation of chol in macrophages.”
Background
Accumulated exposure to high non-high-density lipoprotein cholesterol increases the risk of cardiovascular diseases in hypertensive individuals: An 11-year prospective cohort study
Wu, W., Chen, Y., Wu, K., Zheng, H., Chen, G., Wang, X., Huang, Z., Cai, Z., Cai, Z., Chen, Z., et al. (2023) · Clinical and Experimental Hypertension · doi:10.1080/10641963.2023.2264540 · Cited by 10 · see citing works
Effects of Oxidation on Structural Stability and Remodeling of Human Very Low Density Lipoprotein
Guha, M., & Gursky, O. (2010) · Biochemistry · doi:10.1021/bi101391z · Cited by 10 · see citing works
“This is expected to importantly affect VLDL remodeling and fusion, since even small amounts of lipids with spontaneous negative curvature, such as PE or unsaturated FFA, can accelerate fusion, while those with spontaneous positive curvature such as lysoPC promote fission of small highly curved particles (45, 46).”
Background
Identification of molecular species of cholesteryl ester hydroperoxides in very low-density and intermediate-density lipoproteins
Shrestha, R., Hui, S., Sakurai, T., Yagi, A., Takahashi, Y., Takeda, S., Jin, S., Fuda, H., & Chiba, H. (2013) · Annals of Clinical Biochemistry International Journal of Laboratory Medicine · doi:10.1177/0004563213516093 · Cited by 10 · see citing works
“In previous studies, VLDL remnants are related to oxidation and atherogenicity.(36) In our lipoprotein separation method using ultracentrifugation, remnant lipoproteins cannot be isolated.”
Method
Higher remnant cholesterol increases the risk of coronary heart disease and diabetes in postmenopausal women
Zhang, Y., Song, K., Bi, S., Li, M., & Yao, Z. (2024) · Frontiers in Endocrinology · doi:10.3389/fendo.2024.1475933 · Cited by 9 · see citing works
Two‐Year Changes in Remnant Cholesterol and Stroke Risk in the Chinese Population: A Prospective Cohort Study
Wang, D., Zhang, Z., Zhang, Y., Chen, S., Qu, N., Li, H., Sun, Y., Tian, X., Han, X., Wu, S., et al. (2025) · Journal of the American Heart Association · doi:10.1161/jaha.124.038559 · Cited by 7 · see citing works
Remnant cholesterol is superior to other lipid-related parameters for the prediction of cardiometabolic disease risk in individuals with hypertension: The Kailuan study
Wu, W., Chen, Y., Zhang, C., Wu, K., Zheng, H., Cai, Z., Wang, Y., Fu, P., Lan, Y., Chen, S., et al. (2024) · International Journal of Cardiology · doi:10.1016/j.ijcard.2024.132541 · Cited by 6 · see citing works
Gal-geun-dang-gwi-tang improves diabetic vascular complication in apolipoprotein E KO mice fed a western diet
Lee, S. M., Lee, Y. J., Choi, J. H., Kho, M. C., Yoon, J. J., Shin, S. H., Kang, D. G., & Lee, H. S. (2014) · BMC Complementary and Alternative Medicine · doi:10.1186/1472-6882-14-453 · Cited by 5 · see citing works
“Prior to the appearance of atherosclerotic changes in the vascular wall, a high cholesterol level induces vascular functional changes that may lead to vascular remodelling and increases permeability of LDLcholesterol [29].”
Background
Lipoproteins as biosensors of endothelial oxidative status
Farkas-Epperson, M., & Le, N. (2012) · Clinical Lipidology · doi:10.2217/clp.11.72 · Cited by 4 · see citing works
Determination of the postprandial cut-off value of triglyceride after a daily meal corresponding to fasting optimal triglyceride level in Chinese subjects
Xie, Y., Guo, L., Chen, H., Xu, J. R., Qu, P., Zhu, L., Tan, Y., Zhang, M., Wen, T., & Liu, L. (2023) · Frontiers in Nutrition · doi:10.3389/fnut.2023.1037270 · Cited by 2 · see citing works
“Although TG level is closely associated with RC level, high RC is a more direct risk factor for atherosclerosis compared with high TG because remnant lipoproteins can enter the subendothelial area of the artery and promote the formation of foam cells (18).”
Background
The Role of Remnant Lipoproteins in Atherosclerosis
Kawakami, A., Tanaka, A., Nakano, T., Nakajima, K., & Numano, F. (2000) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2000.tb06337.x · Cited by 2 · see citing works
Cardiometabolic implications of triglyceride–glucose index, remnant cholesterol, and vitamin D in normoglycemic Arab adolescents: a cross-sectional study
Amer, O. E., Sabico, S., Alnaami, A. M., Wani, K., & Al-Daghri, N. (2026) · Frontiers in Endocrinology · doi:10.3389/fendo.2025.1674706 · Cited by 1 · see citing works
Antioxidant and Atherogenic Foam cell Prevention Ability of Methanol and Aqueous Extract ofEmblica OfficinalisFruits and Its Effect onCD36andABCA1Gene Expression in RAW 264.7 Macrophage Cell Line
Nambiar, S. S., & Shetty, N. P. (2014) · Journal of Food Biochemistry · doi:10.1111/jfbc.12089 · Cited by 1 · see citing works
Synthesis of recombinant high density lipoprotein with apolipoprotein A-I and apolipoprotein A-V
Zhang, X., & Chen, B. (2011) · Biological Chemistry · doi:10.1515/bc.2011.041 · Cited by 1 · see citing works
The effects of TG-rich lipoprotein metabolism by oral fat loading, used daily breakfast type oral fat-rich meal “Kisei-meal”
Imamura, K., Maruyama, C., Tsushima, M., Kyotani, S., Nakano, S., NAKAMORI, T., & Maruyama, T. (2001) · The Journal of Japan Atherosclerosis Society · doi:10.5551/jat1973.28.12_205 · Cited by 1 · see citing works
An investigation of the atherogenicity of intermediate density lipoprotein in people with and without type 2 diabetes mellitus
Cheung, C.-L. (2009) · Research Online (University of Wollongong)
Remnant cholesterol is a risk factor for metabolic syndrome and cardiovascular disease: a cross-sectional studyPreprint
Jin, J., Hu, X., François, M., Zeng, P., Wang, W., Yu, B., Zhou, Y., & Dong, H. (2023) · Research Square · doi:10.21203/rs.3.rs-2620348/v1
Regulation of Lipid Homeostasis, Inflammatory Signalling and Atherosclerosis by the Peroxisome Proliferator-Activated Receptor Delta
Bojic, L. A. (2013) · Scholarship@Western (Western University)

Oxidized type IV hypertriglyceridemic VLDL-remnants cause greater macrophage cholesteryl ester accumulation than oxidized LDL
Whitman, S. C., Sawyez, C. G., Miller, D. B., Wolfe, B. M. J., & Huff, M. W. (1998) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)33868-2 · Cited by 51 · see citing works
Self-citation
Oxidized VLDL Induces Less Triglyceride Accumulation in J774 Macrophages Than Native VLDL Due to an Impaired Extracellular Lipolysis
Jong, M. C., Hendriks, W. L., van Vark, L. C., Dahlmans, V. E. H., Groener, J. E. M., & Havekes, L. M. (2000) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.20.1.144 · Cited by 30 · see citing works
Hypertriglyceridemic Very Low Density Lipoproteins Induce Triglyceride Synthesis and Accumulation in Mouse Peritoneal Macrophages
Gianturco, S. H., Bradley, W. A., Gotto, A. M., Morrisett, J. D., & Peavy, D. L. (1982) · Journal of Clinical Investigation · doi:10.1172/jci110590 · Cited by 199 · see citing works
Cholesterol accumulation in J774 macrophages induced by triglyceride-rich lipoproteins. Comparison of very low density lipoprotein from subjects with type III, IV, and V hyperlipoproteinemias.
Huff, M. W., Evans, A. J., Sawyez, C. G., Wolfe, B. M. J., & Nestel, P. J. (1991) · Arteriosclerosis and Thrombosis A Journal of Vascular Biology · doi:10.1161/01.atv.11.2.221 · Cited by 74 · see citing works
Self-citation
Oxidized VLDL Induces Less Triglyceride Accumulation in J774 Macrophages Than Native VLDL Due to an
Havekes, L. M., Jong, M. C., Hendriks, W. L., Vark, L. C. V., Dahlmans, V. E. H., M, J. E., Biol, A. T. V., Lipolysis, I. E., Jong, M. C., Hendriks, W. L., et al. (2015)

Authors: Whitman, S. C., Miller, D. B., Wolfe, B. M., Hegele, R. A., & Huff, M. W.
Affiliations: Western University (CA)
ORCID: Miller, David B.
Hegele, Robert A.
Huff, Murray W.
Venue: Arteriosclerosis, Thrombosis, and Vascular Biology
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 1997-09
Volume: 17
Issue: 9
Pages: 1707-1715
ISSN: 1079-5642 (ISSN-L)
1524-4636
DOI: 10.1161/01.atv.17.9.1707
OpenAlex: W2075141316
Cited by: 59
References: 63
Citations by year: 2026: 1 · 2025: 2 · 2024: 3 · 2023: 5 · 2022: 1 · 2021: 3 · 2020: 4 · 2019: 1 · 2015: 1 · 2014: 3 · 2013: 2 · 2012: 3
FWCI: 3.45
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
PubMed (publishedVersion)
Funders: Heart and Stroke Foundation of Canada
Medical Research Council Canada
Medical Research Council
Topics: Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
Keywords: type III hyperlipoproteinemia, macrophage uptake, cholesteryl ester accumulation, remnant lipoproteins, copper-induced oxidation, LDL oxidation, atherosclerosis, foam cell formation, J774A.1 macrophages, conjugated dienes
MeSH terms: Animals, Cattle, Cell Line, Cells, Cultured, Cholesterol Esters, Electrophoresis, Agar Gel, Foam Cells, Humans, Lipoproteins, LDL, Lipoproteins, VLDL, Macrophages, Oxidation-Reduction, Time Factors, Hypertriglyceridemia, Copper Sulfate, Mice

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

Uptake of type III hypertriglyceridemic VLDL by macrophages is enhanced by oxidation, especially after remnant formation

Abstract

Integrity signals

Claims the paper makes

Claims other papers make about this one

Self-check

Cites

Cited by

Related

Record

About these checks