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Updated: Jun 6, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Complement in atherosclerosis: friend or foe?
W S Speidl1, S P Kastl, K Huber
1Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Insights
The complement system
Area of Science:
- Immunology
- Cardiovascular Research
- Inflammation Biology
Background:
- Atherosclerosis is a chronic inflammatory disease.
- The complement system is crucial for innate immunity and is activated in atherosclerotic plaques.
- The precise role of complement in atherogenesis remains incompletely understood.
Purpose of the Study:
- To review evidence of complement activation in atherosclerotic plaques.
- To discuss the dual role of complement in atherogenesis based on experimental models.
- To summarize complement components as potential biomarkers for cardiovascular disease.
Main Methods:
- Review of existing literature on complement activation in atherosclerosis.
- Analysis of data from experimental animal models of atherosclerosis.
- Synthesis of findings regarding complement's role and biomarker potential.
Main Results:
- Evidence confirms complement activation within atherosclerotic plaques.
- The complement system exhibits a dual role: potentially protective via classic/lectin pathways and proatherogenic via the alternative pathway.
- Anaphylatoxins and terminal complement complex formation may promote plaque destabilization and cardiovascular events.
Conclusions:
- Complement activation is a key feature of atherosclerotic plaques.
- Complement's role in atherogenesis is complex, with both protective and detrimental effects.
- Complement components show promise as biomarkers for cardiovascular disease risk and progression.
Abstract:
Atherosclerosis is a chronic inflammatory disease and the complement system plays a central role in innate immunity. Increasing evidence exists that the complement system is activated within atherosclerotic plaques. However, the role of complement in atherogenesis is not fully understood. Whereas complement activation by the classic and lectin pathway may be protective by removing apoptotic cells and cell debris from atherosclerotic plaques, activation of the complement cascade by the alternative pathway and beyond the C3 convertase with formation of anaphylatoxins and the terminal complement complex may be proatherogenic and may play a role in plaque destabilization leading to its rupture and the onset of acute cardiovascular events. In this review article we present evidence for complement activation within atherosclerotic plaques and we discuss recent data derived from experimental animal models that suggest a dual role of complement in the development of the disease. In addition, we summarize the role of complement components as biomarkers for cardiovascular disease.
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