The DOI matches its Crossref record, with a small difference in title or year; 76 of the 76 references it cites were found in a registry or an index.
Do the Apoe −/− and Ldlr −/– Mice Yield the Same Insight on Atherogenesis?
Open accessAbstract
Murine models of atherosclerosis are useful for investigating the environmental and genetic influences on lesion formation and composition. Apoe −/− and Ldlr −/− mice are the 2 most extensively used models. The models differ in important ways with respect to the precise mechanism by which their absence enhances atherosclerosis, including differences in plasma lipoproteins. The majority of the gene function studies have utilized only 1 model, with the results being generalized to atherogenic mechanisms. In only a relatively few cases have studies been conducted in both atherogenic murine models. This review will discuss important differences between the 2 atherogenic models and will point out studies that have been performed in the 2 models where results are comparable and those where different results were obtained.
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“genetically modified ApoE- and Ldlr-deficient mice have higher plasma cholesterol levels (5 times and 2–3 times higher than controls, respectively) [114]”
From Cardiovascular disease models: A game changing paradigm in drug discovery and screening (2019) · cites this paper as [114]
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Daugherty, A., Tall, A. R., Daemen, M. J. A. P., Falk, E., Fisher, E. A. A., García‐Cardeña, G., Lusis, A. J., Owens, A. P., Rosenfeld, M. E., & Virmani, R. (2017) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atv.0000000000000062 · Cited by 322
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Cardiovascular disease models: A game changing paradigm in drug discovery and screening
Savoji, H., Mohammadi, M. H., Rafatian, N., Toroghi, M. K., Wang, E. Y., Zhao, Y., Korolj, A., Ahadian, S., & Radisic, M. (2019) · Biomaterials · doi:10.1016/j.biomaterials.2018.09.036 · Cited by 223
Metadata
- Authors
- Getz, G. S., & Reardon, C. A.
- Affiliations
- University of Chicago (US)
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2016-09
- Volume
- 36
- Issue
- 9
- Pages
- 1734-1741
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- PMC
- PMC5001905
- OpenAlex
- W2471737803
- Cited by
- 198
- References
- 76
- Citations by year
- 2026: 19 · 2025: 24 · 2024: 20 · 2023: 18 · 2022: 21 · 2021: 19 · 2020: 28 · 2019: 12 · 2018: 19 · 2017: 15 · 2016: 2
- FWCI
- 9.70
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL131028, R01HL088420)
- 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
- atherosclerosis, ApoE-deficient mice, Ldlr knockout mice, atherogenesis, serum lipoproteins, genetic susceptibility to atherosclerosis, model comparison
- MeSH terms
- Animals, Apolipoproteins E, Arteries, Coronary Artery Disease, Disease Models, Animal, Gene Expression Regulation, Lipoproteins, Lymphocytes, Macrophages, Phenotype, Receptors, LDL, Biomarkers, Mice, Knockout, Genetic Predisposition to Disease, Atherosclerosis, Plaque, Atherosclerotic, Diet, High-Fat
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