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Atherosclerosis Drug Discovery

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Cholesterol can be controlled

New Password. The thrust of material is centered around animal models useful as tools in the search and evaluation of new drugs.

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Broadly categorized, the models are nonhuman primates, rabbits, rodents, quail, and tissue culture. The material is a mix of studies on serum lipids and, more importantly, of studies on the artery, irrespective of serum lipid levels. The prevention of arterial lesions, not reduction of serum lipids, is emphasized. A review of all anti-atherosclerotic agents, with the exception of hypolipidemic agents, is included in this volume of the proceedings of the symposium. JavaScript is currently disabled, this site works much better if you enable JavaScript in your browser.

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Abstract Atherosclerosis is the leading cause of death worldwide. To date, the use of statins to lower LDL levels has been the major intervention used to delay or halt disease progression. These drugs have an incomplete impact on plaque burden and risk, however, as evidenced by the substantial rates of myocardial infarctions that occur in large-scale clinical trials of statins.

Thus, it is hoped that by understanding the factors that lead to plaque regression, better approaches to treating atherosclerosis may be developed. A transplantation-based mouse model of atherosclerosis regression has been developed by allowing plaques to form in a model of human atherosclerosis, the apoE-deficient mouse, and then placing these plaques into recipient mice with a normolipidemic plasma environment.

Under these conditions, the depletion of foam cells occurs.


Interestingly, the disappearance of foam cells was primarily due to migration in a CCR7-dependent manner to regional and systemic lymph nodes after 3 days in the normolipidemic regression environment. Further studies using this transplant model demonstrated that liver X receptor and HDL are other factors likely to be involved in plaque regression. In conclusion, through the use of this transplant model, the process of uncovering the pathways regulating atherosclerosis regression has begun, which will ultimately lead to the identification of new therapeutic targets.


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