Do the Apoe −/− and Ldlr −/– Mice Yield the Same Insight on Atherogenesis?
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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-deficient mice have plasma cholesterol about five times higher than controls, and Ldlr-deficient mice have levels two to three times higher.
“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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- 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
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Surgery › 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
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 ›
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