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The ApoE /– phenotype is an experimental model for atherosclerosis in humans.
Our previously published theoretical model for atherosclerosis formation can help us to design novel therapeutic strategies by which coronary atherosclerosis is controlled more efficiently.
Therefore, we examined the extent to how VSL#3 reduced atherosclerosis, the cardiovascular inflammation, and the effects of VSL#3 on the gut satiety hormones, inflammatory profile and the changes in the gut microbial community in apolipoprotein E knockout (ApoE−/−) mice, a well-established and popular model for atherosclerosis (Meir and Leitersdorf 2004).
Four groups of ApoE*3Leiden mice, a humanized model for atherosclerosis, were subjected to different feeding treatments for 16 weeks.
Additionally, rabbits are a well-established model for atherosclerosis.
ApoE−/− mouse is a widely used animal model for atherosclerosis study.
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Imaging with labeled nanobodies has proven its value in preclinical models for atherosclerosis and tumors.
Rats, rabbits, dogs, pigs, and monkeys are well-established animal models for atherosclerosis, and thrombosis.
Shortly after this observation, mouse models for atherosclerosis revealed a role for CXCL10 in (early) lesion development.
Using a combination of existing murine models for atherosclerosis and sepsis, we found that CLP, a model of intra-abdominal sepsis, accelerates atheroma development.
In regard to vascular biology in particular, TNFR2 seems to be crucial for both TNFα-induced atherosclerotic lesions in mouse models for atherosclerosis [ 39- 41] and leukocyte interaction with the endothelium [ 42].
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