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Updated: May 1, 2026

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
Regression of atherosclerosis: insights from animal and clinical studies
1Zena and Michael A. Wiener Cardiovascular Institute, Mount Sinai Medical Center, New York, NY.
Background:
Based on studies that date back to the 1920s, regression and stabilization of atherosclerosis in humans has gone from just a dream to one that is achievable. Review of the literature indicates that the successful attempts at regression generally applied robust measures to improve plasma lipoprotein profiles. Examples include extensive lowering of plasma concentrations of atherogenic apolipoprotein B and enhancement of reverse cholesterol transport from atheromata to the liver.
Findings:
Possible mechanisms responsible for lesion shrinkage include decreased retention of atherogenic apolipoprotein B within the arterial wall, efflux of cholesterol and other toxic lipids from plaques, emigration of lesional foam cells out of the arterial wall, and influx of healthy phagocytes that remove necrotic debris as well as other components of the plaque. This review will highlight the role key players such as LXR, HDL and CCR7 have in mediating regression.
Conclusion:
Although much progress has been made, there are many unanswered questions. There is, therefore, a clear need for preclinical and clinical testing of new agents expected to facilitate atherosclerosis regression with the hope that additional mechanistic insights will allow further progress.
Insights
Atherosclerosis regression is achievable through improved lipoprotein profiles, lowering atherogenic apolipoprotein B, and enhancing reverse cholesterol transport. Further research is needed to develop new agents and gain mechanistic insights for effective treatment.
Area of Science:
- Cardiovascular Science
- Molecular Biology
- Biochemistry
Background:
- Atherosclerosis regression, once a distant goal, is now attainable based on research since the 1920s.
- Successful regression strategies involve significant improvements in plasma lipoprotein profiles.
- Key interventions include reducing atherogenic apolipoprotein B and boosting reverse cholesterol transport.
Purpose of the Study:
- To review the mechanisms and key molecular players involved in atherosclerosis regression.
- To highlight the roles of Liver X Receptor (LXR), High-Density Lipoprotein (HDL), and CCR7 in mediating plaque regression.
Main Methods:
- Literature review of studies on atherosclerosis regression.
- Analysis of mechanisms contributing to atherosclerotic lesion shrinkage.
- Identification of molecular mediators of regression.
Main Results:
- Mechanisms for lesion shrinkage include reduced retention of apolipoprotein B, lipid efflux from plaques, foam cell emigration, and infiltration of phagocytes.
- Key molecular players like LXR, HDL, and CCR7 are crucial in mediating regression processes.
- Studies demonstrate that improving lipoprotein profiles is central to achieving atherosclerosis regression.
Conclusions:
- Significant advancements have been made in understanding atherosclerosis regression.
- Unanswered questions necessitate further preclinical and clinical investigations.
- Developing novel agents and gaining deeper mechanistic insights are vital for future progress in treating atherosclerosis.
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