The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
ApoE-deficient mice develop lesions of all phases of atherosclerosis throughout the arterial tree.
Abstract
Initial description of apolipoprotein (apo) E-deficient transgenic mice demonstrated the development of severe hypercholesterolemia due to probable delayed clearance of large atherogenic particles from the circulation. Examination of these mice demonstrated foam cell accumulation in the aortic root and pulmonary arteries by 10 weeks of age. In the present study, the animals were fed either chow or a high-fat, Western-type diet and examined at ages ranging from 6 to 40 weeks. Gross examination by dissection microscopy revealed a predilection for development of lesions in the aortic root, at the lesser curvature of the aortic arch, the principal branches of the aorta, and in the pulmonary and carotid arteries. Monocyte attachment to endothelial cells was observed by light and electron microscopic examination at 6 weeks, the earliest time point examined. Foam cell lesions developed as early as 8 weeks, and after 15 weeks advanced lesions (fibrous plaques) were observed. The latter consisted of a fibrous cap containing smooth muscle cells surrounded by connective tissue matrix that covered a necrotic core with numerous foamy macrophages. Mice fed the Western-type diet generally had more advanced lesions than those fed a chow diet. The apoE-deficient mouse contains the entire spectrum of lesions observed during atherogenesis and is the first mouse model to develop lesions similar to those in humans. This model should provide numerous opportunities to study the pathogenesis and therapy of atherosclerosis in a small, genetically defined animal.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
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?
In the citing paper
“Apo E knockout mice are considered to be one of the most relevant models for atherosclerosis because they are hypercholesterolemic and develop spontaneous arterial lesions (87).”
From Trimethylamine N -Oxide, the Microbiome, and Heart and Kidney Disease (2017) · cites this paper as [87]
Citations
Cites
The pathogenesis of atherosclerosis: a perspective for the 1990s
Ross, R. (1993) · Nature · doi:10.1038/362801a0 · Cited by 10,618
Self-citationPlump, 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-citationSpontaneous Hypercholesterolemia and Arterial Lesions in Mice Lacking Apolipoprotein E
Zhang, S. H., Reddick, R. L., Piedrahita, J. A., & Maeda, N. (1992) · Science · doi:10.1126/science.1411543 · Cited by 2,237
Rg, G. (1981) · PubMed Central · Cited by 1,314
Faggiotto, A., Ross, R., & Harker, L. A. (1984) · Arteriosclerosis An Official Journal of the American Heart Association Inc · doi:10.1161/01.atv.4.4.323 · Cited by 978
Self-citationGown, A. M., Tsukada, T., & Ross, R. (1986) · PubMed · Cited by 678
Self-citationFaggiotto, A., & Ross, R. (1984) · Arteriosclerosis An Official Journal of the American Heart Association Inc · doi:10.1161/01.atv.4.4.341 · Cited by 466
Self-citationThe role of the monocyte in atherogenesis: II. Migration of foam cells from atherosclerotic lesions.
Gerrity, R. G. (1981) · PubMed · Cited by 459
Severe atherosclerosis in transgenic mice expressing simian cholesteryl ester transfer protein
Marotti, K. R., Castle, C. K., Boyle, T. P., Lin, A. H., Murray, R. W., & Melchior, G. W. (1993) · Nature · doi:10.1038/364073a0 · Cited by 444
Atherosclerosis in Transgenic Mice Overexpressing Apolipoprotein A-II
Warden, C. H., Hedrick, C. C., Qiao, J.-H., Castellani, L. W., & Lusis, A. J. (1993) · Science · doi:10.1126/science.8332912 · Cited by 359
Cited by
Sorted by citations
Atherosclerosis--an inflammatory disease
Ross, R. (1999) · New England Journal of Medicine · doi:10.1056/nejm199901143400207 · Cited by 21,725
Self-citationMolecular Regulation of Vascular Smooth Muscle Cell Differentiation in Development and Disease
Owens, G. K., Kumar, M. S., & Wamhoff, B. R. (2004) · Physiological Reviews · doi:10.1152/physrev.00041.2003 · Cited by 3,472
Chiu, J.-J., & Chien, S. (2011) · Physiological Reviews · doi:10.1152/physrev.00047.2009 · Cited by 2,280
Spontaneous calcification of arteries and cartilage in mice lacking matrix GLA protein
Luo, G., Ducy, P. F., McKee, M. D., Pinero, G. J., Loyer, E. M., Behringer, R. R., & Karsenty, G. (1997) · Nature · doi:10.1038/386078a0 · Cited by 2,118
Boring, L., Gosling, J., Cleary, M., & Charo, I. F. (1998) · Nature · doi:10.1038/29788 · Cited by 1,965
Metadata
- Authors
- Nakashima, Y., Plump, A. S., Raines, E. W., Breslow, J. L., & Ross, R.
- Affiliations
- University of Washington (US)
- Venue
- Arteriosclerosis and Thrombosis: A Journal of Vascular Biology
- Published
- 1994-01
- Volume
- 14
- Issue
- 1
- Pages
- 133-140
- ISSN
- 1049-8834 (ISSN-L)
- OpenAlex
- W1964814612
- Cited by
- 1,693
- References
- 28
- Citations by year
- 2026: 18 · 2025: 32 · 2024: 40 · 2023: 42 · 2022: 54 · 2021: 60 · 2020: 47 · 2019: 57 · 2018: 45 · 2017: 66 · 2016: 50 · 2015: 69 · 2014: 71 · 2013: 73 · 2012: 78
- FWCI
- 14.99
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Arteriosclerosis and Thrombosis A Journal of Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Bristol-Myers Squibb
- National Institutes of Health (5r01hl033714-17, 18645, HL 18645)
- National Heart, Lung, and Blood Institute (HL-18645, HL 33714, R01HL032435, HL32435, P01HL018645)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Keywords
- apolipoprotein E deficiency, atherosclerosis, atherosclerotic plaque development, Western diet, hypercholesterolemia, fibrous cap, necrotic core, aortic root lesions, mouse model of atherosclerosis, atherogenesis
- MeSH terms
- Animals, Aorta, Aorta, Thoracic, Apolipoproteins E, Arteriosclerosis, Carotid Arteries, Coronary Vessels, Diet, Endothelium, Vascular, Hypercholesterolemia, Leukocytes, Mononuclear, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Transgenic, Microscopy, Electron, Pulmonary Artery, 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
