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Role of complement activation in atherosclerosis.
Riina Oksjoki1, Petri T Kovanen, Markku O Pentikäinen
1Wihuri Research Institute, Helsinki, Finland.
Current Opinion in Lipidology
|September 23, 2003
Summary
The complement system, a key inflammatory factor in atherosclerosis, shows activation in human lesions. However, studies in hyperlipidemic mice suggest a limited role for complement in experimental atherogenesis.
Area of Science:
- Immunology
- Cardiovascular Research
- Inflammation Biology
Background:
- Atherosclerosis involves significant inflammation within the arterial intima.
- The complement system is a critical component of the innate immune system implicated in inflammatory processes.
Purpose of the Study:
- To review recent advancements in understanding the complement system's role in atherogenesis.
- To explore the connection between complement activation and the development of atherosclerotic lesions.
Main Methods:
- Review of current literature on complement system activation in atherosclerosis.
- Analysis of findings from human atherosclerotic lesions.
- Evaluation of experimental data from genetically engineered hyperlipidemic mouse models.
Main Results:
- The complement system is demonstrably activated in human atherosclerotic lesions.
- Triggers include immunocomplexes, C-reactive protein, modified lipoproteins, apoptotic cells, and cholesterol crystals.
- Anaphylatoxin receptors are present in human lesions, but mouse models show limited complement involvement in experimental atherogenesis.
Conclusions:
- Human studies provide substantial circumstantial evidence linking complement to atherosclerosis.
- Recent findings in hyperlipidemic mouse models present a contrasting view, indicating a modest or negative role for complement in experimental atherogenesis.