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Updated: Jun 3, 2026

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
Pharmacological modulation of cell death in atherosclerosis: a promising approach towards plaque stabilization?
Wim Martinet1, Dorien M Schrijvers, Guido R Y De Meyer
1Division of Pharmacology, University of Antwerp, Antwerp, Belgium. wim.martinet@ua.ac.be
Abstract:
Despite tremendous advances over the last 15 years in identifying vulnerable atherosclerotic plaques, the incidence of death and disability caused by such lesions still remains the number one health threat in developed countries. Therefore, new systemic or focal therapies aimed at decreasing the overall burden of disease, and a change to a more benign phenotype, are needed. Because cell death is a prominent feature of advanced atherosclerotic plaques with a major impact on plaque destabilization, an increasing number of compounds targeting the apoptotic or autophagic machinery in atherosclerosis are being explored, predominantly at the preclinical level. This review will provide an overview of these compounds, with a focus on both inhibition and stimulation of cell death, to prevent acute coronary syndromes and sudden cardiac death.
Insights
Targeting cell death pathways in atherosclerosis is crucial for developing new therapies. This review explores compounds that inhibit or stimulate cell death to prevent heart attacks and sudden cardiac death.
Area of Science:
- Cardiovascular Research
- Cell Biology
- Pharmacology
Background:
- Atherosclerosis remains a leading cause of death and disability globally.
- Vulnerable atherosclerotic plaques are a major concern, necessitating novel therapeutic strategies.
- Cell death significantly contributes to plaque destabilization and adverse cardiovascular events.
Purpose of the Study:
- To review emerging compounds targeting cell death pathways in atherosclerosis.
- To explore therapeutic strategies involving both inhibition and stimulation of cell death.
- To provide insights into preventing acute coronary syndromes and sudden cardiac death.
Main Methods:
- Literature review of preclinical studies on compounds affecting apoptosis and autophagy in atherosclerosis.
- Analysis of therapeutic approaches targeting cell death mechanisms.
- Synthesis of current research on systemic and focal therapies.
Main Results:
- Numerous compounds targeting apoptotic and autophagic machinery are under preclinical investigation.
- Both inhibition and stimulation of cell death show potential in preclinical models.
- Therapeutic interventions aim to shift plaque phenotype towards stability.
Conclusions:
- Targeting cell death pathways represents a promising therapeutic avenue for atherosclerosis.
- Further research is needed to translate preclinical findings into clinical applications.
- Modulating cell death could significantly reduce the burden of cardiovascular disease.
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