The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Mouse Models of Atherosclerosis
Abstract
As a species the mouse is highly resistant to atherosclerosis. However, through induced mutations it has been possible to develop lines of mice that are susceptible to this disease. For example, mice that are deficient in apolipoprotein E, a ligand important in lipoprotein clearance, develop atherosclerotic lesions resembling those observed in humans. These lesions are exacerbated when the mice are fed a high-cholesterol, high-fat, Western-type diet. Other promising models are mice that are deficient in the low density lipoprotein receptor and transgenic mice that express human apolipoprotein B and transdominant mutant forms of apolipoprotein E. These models are now being used to study the pathogenesis of atherosclerotic lesions, as well as the influence of genetics, environment, hormones, and drugs on lesion development.
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“Indeed, many of the mouse models for genetic AD that harbour different human APP mutations have also been shown to exhibit CAA [49], [50], although the overexpression of APP alone causes no Aβ deposition in most mouse lines [51], and mouse app does not generate amyloid plaques.”
From ApoB100/LDLR-/- Hypercholesterolaemic Mice as a Model for Mild Cognitive Impairment and Neuronal Damage (2011) · cites this paper as [49]
In the citing paper
“Interestingly, the present transgenic mice showed early cerebrovascular β-amyloidosis that was exacerbated with age, in the same way that, in human mutant APP mouse models, a close relationship is seen between high plasma cholesterol and brain vessel amyloidosis [49], [50].”
From ApoB100/LDLR-/- Hypercholesterolaemic Mice as a Model for Mild Cognitive Impairment and Neuronal Damage (2011) · cites this paper as [49]
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Cites
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
Self-citationApoE-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
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Research works printed but not linked: 31
- BELLOSTA S, MACROPHAGE-SPECIFIC EXPRESSION OF HUMAN APOLIPOPROTEIN-E REDUCES ATHEROSCLEROSIS IN HYPERCHOLESTEROLEMIC APOLIPOPROTEIN E-NULL MICE, JOURNAL OF CLINICAL INVESTIGATION 96, 2170 (1995). · DOI · Paper page
- BOISVERT W.A., TREATMENT OF SEVERE HYPERCHOLESTEROLEMIA IN APOLIPOPROTEIN E-DEFICIENT MICE BY BONE-MARROW TRANSPLANTATION, JOURNAL OF CLINICAL INVESTIGATION 96, 1118 (1995). · DOI
- CALLOW M.J., ATHEROGENESIS IN TRANSGENIC MICE WITH HUMAN APOLIPOPROTEIN-B AND LIPOPROTEIN (A), JOURNAL OF CLINICAL INVESTIGATION 96, 1639 (1995). · DOI
- FAZIO S, SUSCEPTIBILITY TO DIET-INDUCED ATHEROSCLEROSIS IN TRANSGENIC MICE EXPRESSING A DYSFUNCTIONAL HUMAN APOLIPOPROTEIN E(ARG 112,CYS142), ARTERIOSCLEROSIS AND THROMBOSIS 14, 1873 (1994). · DOI
- HAYEK T, DECREASED EARLY ATHEROSCLEROTIC LESIONS IN HYPERTRIGLYCERIDEMIC MICE EXPRESSING CHOLESTERYL ESTER TRANSFER PROTEIN TRANSGENE, JOURNAL OF CLINICAL INVESTIGATION 96, 2071 (1995). · DOI
- ISHIBASHI S, MASSIVE XANTHOMATOSIS AND ATHEROSCLEROSIS IN CHOLESTEROL-FED LOW-DENSITY-LIPOPROTEIN RECEPTOR-NEGATIVE MICE, JOURNAL OF CLINICAL INVESTIGATION 93, 1885 (1994). · DOI
- LAWN R.M., ATHEROGENESIS IN TRANSGENIC MICE EXPRESSING HUMAN APOLIPOPROTEIN(A), NATURE 360, 670 (1992). · DOI
- LIAO F, GENETIC-CONTROL OF INFLAMMATORY GENE INDUCTION AND NF-KAPPA-B-LIKE TRANSCRIPTION FACTOR ACTIVATION IN RESPONSE TO AN ATHEROGENIC DIET IN MICE, JOURNAL OF CLINICAL INVESTIGATION 91, 2572 (1993). · DOI
- LINTON M.F., PREVENTION OF ATHEROSCLEROSIS IN APOLIPOPROTEIN E-DEFICIENT MICE BY BONE-MARROW TRANSPLANTATION, SCIENCE 267, 1034 (1995). · DOI · Paper page
- MANCINI F.P., RELATIVE CONTRIBUTIONS OF APOLIPOPROTEIN(A) AND APOLIPOPROTEIN-B TO THE DEVELOPMENT OF FATTY LESIONS IN THE PROXIMAL AORTA OF MICE, ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY 15, 1911 (1995). · DOI
- MAROTTI K.R., SEVERE ATHEROSCLEROSIS IN TRANSGENIC MICE EXPRESSING SIMIAN CHOLESTERYL ESTER TRANSFER PROTEIN, NATURE 364, 73 (1993). · DOI
- 10.1016/0021-9150(85)90138-8 · DOI
- PAIGEN B, ATH-1, A GENE DETERMINING ATHEROSCLEROSIS SUSCEPTIBILITY AND HIGH-DENSITY-LIPOPROTEIN LEVELS IN MICE, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 84, 3763 (1987). · DOI
- PALINSKI W, INCREASED AUTOANTIBODY TITERS AGAINST EPITOPES OF OXIDIZED LDL IN LDL RECEPTOR-DEFICIENT MICE WITH INCREASED ATHEROSCLEROSIS, ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY 15, 1569 (1995). · DOI
- PALINSKI W, 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, ARTERIOSCLEROSIS AND THROMBOSIS 14, 605 (1994). · DOI
- PASZTY C, APOLIPOPROTEIN AI TRANSGENE CORRECTS APOLIPOPROTEIN-E DEFICIENCY-INDUCED ATHEROSCLEROSIS IN MICE, JOURNAL OF CLINICAL INVESTIGATION 94, 899 (1994). · DOI
- PLUMP A.S., CIRCULATION 88, A9 (1993).
- PLUMP A.S., HUMAN APOLIPOPROTEIN-A-I GENE-EXPRESSION INCREASES HIGH-DENSITY-LIPOPROTEIN AND SUPPRESSES ATHEROSCLEROSIS IN THE APOLIPOPROTEIN E-DEFICIENT MOUSE, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 91, 9607 (1994). · DOI
- PURCELLHUYNH D.A., TRANSGENIC MICE EXPRESSING HIGH-LEVELS OF HUMAN APOLIPOPROTEIN-B DEVELOP SEVERE ATHEROSCLEROTIC LESIONS IN RESPONSE TO A HIGH-FAT DIET, JOURNAL OF CLINICAL INVESTIGATION 95, 2246 (1995). · DOI
- REDDICK R.L., ATHEROSCLEROSIS IN MICE LACKING APO-E - EVALUATION OF LESIONAL DEVELOPMENT AND PROGRESSION, ARTERIOSCLEROSIS AND THROMBOSIS 14, 141 (1994). · DOI · Paper page
- RUBIN E.M., INHIBITION OF EARLY ATHEROGENESIS IN TRANSGENIC MICE BY HUMAN APOLIPOPROTEIN-A-I, NATURE 353, 265 (1991). · DOI
- SCHULTZ J.R., PROTEIN-COMPOSITION DETERMINES THE ANTI-ATHEROGENIC PROPERTIES OF HDL IN TRANSGENIC MICE, NATURE 365, 762 (1993). · DOI
- SHIMANO H, INHIBITION OF DIET-INDUCED ATHEROMA FORMATION IN TRANSGENIC MICE EXPRESSING APOLIPOPROTEIN-E IN THE ARTERIAL-WALL, JOURNAL OF CLINICAL INVESTIGATION 95, 469 (1995). · DOI
- SMITH J.D., DECREASED ATHEROSCLEROSIS IN MICE DEFICIENT IN BOTH MACROPHAGE-COLONY-STIMULATING FACTOR (OP) AND APOLIPOPROTEIN-E, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 92, 8264 (1995). · DOI
- TANGIRALA R.K., EFFECT OF THE ANTIOXIDANT N,N'-DIPHENYL 1,4-PHENYLENEDIAMINE (DPPD) ON ATHEROSCLEROSIS IN APOE-DEFICIENT MICE, ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY 15, 1625 (1995). · DOI
- TANGIRALA R.K., QUANTITATION OF ATHEROSCLEROSIS IN MURINE MODELS - CORRELATION BETWEEN LESIONS IN THE AORTIC ORIGIN AND IN THE ENTIRE AORTA, AND DIFFERENCES IN THE EXTENT OF LESIONS BETWEEN SEXES IN LDL RECEPTOR-DEFICIENT AND APOLIPOPROTEIN E-DEFICIENT MICE, JOURNAL OF LIPID RESEARCH 36, 2320 (1995). · DOI
- VANREE J.H., DIET-INDUCED HYPERCHOLESTEROLEMIA AND ATHEROSCLEROSIS IN HETEROZYGOUS APOLIPOPROTEIN E-DEFICIENT MICE, ATHEROSCLEROSIS 111, 25 (1994). · DOI
- VANVLIJMEN BJM, DIET-INDUCED HYPERLIPOPROTEINEMIA AND ATHEROSCLEROSIS IN APOLIPOPROTEIN E3 LEIDEN TRANSGENIC MICE, JOURNAL OF CLINICAL INVESTIGATION 93, 1403 (1994). · DOI
- 10.1126/science.8332912 · DOI
- ZHANG S.H., DIET-INDUCED ATHEROSCLEROSIS IN MICE HETEROZYGOUS AND HOMOZYGOUS FOR APOLIPOPROTEIN-E GENE DISRUPTION, JOURNAL OF CLINICAL INVESTIGATION 94, 937 (1994). · DOI
- 10.1126/science.1411543 · DOI · Paper page
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Metadata
- Authors
- Breslow, J. L.
- Affiliations
- The author is in the Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York, NY 10021, USA.
- Venue
- Science
- Published
- 1996-05-03
- Volume
- 272
- Issue
- 5262
- Pages
- 685-688
- ISSN
- 0036-8075
- 1095-9203
- Cited by
- 549
- References
- 2
- Language
- en
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