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Updated: Apr 4, 2026

Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
ApoA-I-Directed Therapies for the Management of Atherosclerosis
1Division of Translational Medicine and Human Genetics, Perelman School of Medicine at the University of Pennsylvania, 3400 Civic Center Blvd, Room 11-132, Philadelphia, PA, 19104, USA, jsmillar@upenn.edu.
Insights
Recent studies question high-density lipoprotein cholesterol
Area of Science:
- Cardiovascular Research
- Pharmacology
- Biochemistry
Background:
- Recent reports challenge the established atheroprotective role of high-density lipoprotein cholesterol (HDL-C).
- Despite these doubts, significant research supports targeting HDL function for therapeutic benefit.
- Focus is shifting from increasing HDL-C levels to enhancing HDL's functional capacity.
Purpose of the Study:
- To review pharmacological strategies aimed at improving HDL function.
- To explore interventions targeting apolipoprotein A-I (apoA-I) for atherosclerotic risk reduction.
- To discuss novel therapeutic approaches for cardiovascular disease.
Main Methods:
- Review of scientific literature on HDL-C and cardiovascular risk.
- Analysis of pharmacological interventions targeting HDL function.
- Categorization of interventions into small molecule pharmaceuticals, mimetic peptides, and apoA-I infusions.
Main Results:
- Development of diverse pharmacological agents that modulate HDL function.
- Identification of small molecule drugs, HDL mimetic peptides, and apoA-I infusions as key strategies.
- Evidence supporting the potential of these interventions in managing atherosclerosis.
Conclusions:
- Pharmacological enhancement of HDL function, rather than simply increasing HDL-C levels, shows promise.
- Targeting apoA-I and HDL function represents a viable therapeutic avenue for reducing atherosclerotic risk.
- Future research should focus on the clinical efficacy of these novel HDL-targeting agents.
Abstract:
Several recent reports have raised doubts about the atheroprotective role of high-density lipoprotein cholesterol (HDL-C). Nevertheless, a substantial body of work supports the validity of pharmacological interventions able to enhance HDL function, as opposed to raising HDL-C levels per se. In this article, we briefly review the development of pharmacological interventions that target apoA-I and HDL function as a means of reducing atherosclerotic risk: small molecule pharmaceuticals, small HDL mimetic peptides, and infusion of apoA-I-containing particles.
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