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Updated: Jul 2, 2026
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A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Apoptosis in atherosclerosis: a mini-review.
Maria Karaflou1, Irene Lambrinoudaki, George Christodoulakos
12nd Department of Obstetrics and Gynecology, University of Athens, Aretaieion Hospital, 27 Themistokleous Street, Dionysos, Athens, Greece. ilambrinoudaki@hotmail.com
Mini Reviews in Medicinal Chemistry
|August 12, 2008
Summary
Apoptosis, programmed cell death, plays a dual role in atherosclerosis. While it can initially slow the disease by eliminating inflammatory cells, it promotes plaque instability and rupture in later stages.
Area of Science:
- Cardiovascular Biology
- Cellular Pathology
- Immunology
Background:
- Atherosclerosis involves complex inflammatory processes.
- Apoptosis (programmed cell death) is implicated in lesion development.
- Triggers include cell-cell contact, cytokines, and oxidized lipids.
Purpose of the Study:
- To elucidate the multifaceted role of apoptosis in atherogenesis.
- To differentiate the impact of apoptosis based on atherosclerotic plaque stage.
Main Methods:
- Review and synthesis of existing literature on apoptosis in atherosclerosis.
- Analysis of cellular and molecular mechanisms driving apoptosis in atherosclerotic lesions.
Main Results:
- Early-stage apoptosis of smooth muscle cells, lymphocytes, and macrophages may inhibit atherogenesis.
- Late-stage apoptosis contributes to plaque instability, rupture, and thrombosis.
Conclusions:
- Apoptosis exhibits a context-dependent role in atherosclerosis progression.
- Understanding apoptosis is crucial for developing targeted therapies for atherosclerotic cardiovascular disease.
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