The DOI matches its Crossref record; 178 of the 178 references it cites were found in a registry or an index.
Animal Models of Atherosclerosis
Open accessAbstract
Atherosclerosis is a chronic inflammatory disorder that is the underlying cause of most cardiovascular disease. Both cells of the vessel wall and cells of the immune system participate in atherogenesis. This process is heavily influenced by plasma lipoproteins, genetics, and the hemodynamics of the blood flow in the artery. A variety of small and large animal models have been used to study the atherogenic process. No model is ideal as each has its own advantages and limitations with respect to manipulation of the atherogenic process and modeling human atherosclerosis or lipoprotein profile. Useful large animal models include pigs, rabbits, and nonhuman primates. Due in large part to the relative ease of genetic manipulation and the relatively short time frame for the development of atherosclerosis, murine models are currently the most extensively used. Although not all aspects of murine atherosclerosis are identical to humans, studies using murine models have suggested potential biological processes and interactions that underlie this process. As it becomes clear that different factors may influence different stages of lesion development, the use of mouse models with the ability to turn on or delete proteins or cells in tissue specific and temporal manner will be very valuable.
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Cites
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Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease
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Identification of splenic reservoir monocytes and their deployment to inflammatory sites
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ApoE-deficient mice develop lesions of all phases of atherosclerosis throughout the arterial tree.
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“) A thorough pathological analysis of the evolution of atherosclerosis in apoE mice fed either chow or WTD represents the best systematic analysis of lesion development in mice.(54) Lesions developed in the aortic root, the innominate artery (brachiocephalic) and other branches of the aorta, as well as the pulmonary a…”
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Cited by
Animal models of atherosclerosis
Emini Veseli, B., Perrotta, P., De Meyer, G. R. A., Roth, L., Van der Donckt, C., Martinet, W., & De Meyer, G. R. Y. (2017) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2017.05.010 · Cited by 548
Atherosclerosis: Known and unknown
Fan, J., & Watanabe, T. (2022) · Pathology International · doi:10.1111/pin.13202 · Cited by 523
Cytokines in atherosclerosis: Key players in all stages of disease and promising therapeutic targets
Ramji, D. P., & Davies, T. S. (2015) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2015.04.003 · Cited by 469
Shared molecular and cellular mechanisms of premature ageing and ageing-associated diseases
Kubben, N., & Misteli, T. (2017) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm.2017.68 · Cited by 320
Fan, J., Kitajima, S., Watanabe, T., Xu, J., Zhang, J., Liu, E., & Chen, Y. E. (2015) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2014.09.009 · Cited by 333
Metadata
- Authors
- Getz, G. S., & Reardon, C. A.
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2012-05
- Volume
- 32
- Issue
- 5
- Pages
- 1104-1115
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W2098486305
- Cited by
- 630
- References
- 178
- FWCI
- 14.17
- Type
- journal article
- Language
- en
- Open access
- bronze
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
