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Genes potentially involved in plaque rupture.
Birgit C G Faber1, Sylvia Heeneman, Mat J A P Daemen
1Department of Pathology, Cardiovascvular Research Institute Maastricht (CARIM), University of Maastricht, 6200 MD Maastricht, The Netherlands.
Current Opinion in Lipidology
|September 28, 2002
Summary
Atherosclerotic plaque rupture, a key event in heart attack and stroke, involves complex gene expression. Targeting multiple molecular mechanisms simultaneously may offer the most effective interventions for plaque rupture.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Genomics
Background:
- Atherosclerotic plaque rupture is the primary cause of acute coronary syndromes and stroke.
- The molecular mechanisms underlying plaque rupture remain incompletely understood.
- Advancements in gene expression profiling techniques allow for the study of atherogenesis.
Purpose of the Study:
- To review recent large-scale gene expression profiles from whole mount vascular specimens.
- To elucidate the molecular mechanisms involved in atherosclerotic plaque rupture.
Main Methods:
- Analysis of gene expression profiles from whole mount vascular tissue.
- Utilizing techniques such as microarray, suppression subtractive hybridization, and differential display.
- Evaluation of animal models exhibiting plaque rupture phenotypes.
Main Results:
- Gene expression profiles identified three key mechanisms in plaque rupture: extracellular matrix turnover, cell turnover regulation, and lipid metabolism.
- Animal models confirmed the involvement of these three mechanisms.
- Interventions targeting at least two mechanisms in mouse models produced the most significant phenotypes.
Conclusions:
- Plaque rupture is a multifactorial process, as evidenced by recent mouse models.
- Therapeutic strategies may be most effective when they address multiple underlying mechanisms of plaque rupture simultaneously.