Molecular genetics of coronary artery disease.
PURPOSE OF REVIEW: Coronary artery disease, including its most severe complication myocardial infarction, is the leading cause of death; however, its genetic studies lag behind other diseases. Many advances have recently been made, however, and these are reviewed here. RECENT FINDINGS: Positional cloning based on genome-wide linkage analysis with large families identified the first non - lipid-related disease-causing gene, MEF2A (encoding a transcriptional factor), for coronary artery disease and myocardiaI infarction. The MEF2A mutations may account for up to 1.93% of the disease population; thus, genetic testing based on mutational analysis of MEF2A may soon be available for many coronary artery disease/myocardial infarction patients. Genome-wide association studies identified significant association for myocardiaI infarction with the LTA gene (encoding lymphotoxin-alpha), and a follow-up study found that an LTA-interacting gene, LGALS2 (encoding galectin-2), is also a susceptibility gene for myocardiaI infarction. Studies that employ genome-wide linkage scans with hundreds of small nuclear families have identified new susceptibility genes for coronary artery disease and myocardiaI infarction, including ALOX5AP (encoding 5-lipoxygenase-activating protein) associated with myocardial infarction and stroke and PDE4D (encoding phosphodiesterase 4D) for ischemic stroke. SUMMARY: Genetic studies provide new insights into the pathogenesis of coronary artery disease and myocardial infarction. Future studies will focus on identification of new disease-causing genes and susceptibility genes, exploration of the molecular mechanisms by which mutations cause coronary artery disease/myocardiaI infarction, and gene-specific therapies for patients.[1]References
- Molecular genetics of coronary artery disease. Wang, Q. Curr. Opin. Cardiol. (2005) [Pubmed]
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