This review outlines a contemporary research paradigm for studying the genetics of coronary artery disease to define functional mutations and gene-environment interactions.
Guides CAD genetic research design; leaves open clinical translation of functional mutations and gene-environment interactions.
Rapid discoveries of novel and unexpected disease-associated genes for atherosclerotic coronary artery disease (CAD) are anticipated as genomic maps become more detailed and methods for mapping complex disease phenotypes become more refined. Although establishing association or linkage of a marker locus to a CAD susceptibility gene is an important first step, the long-term goal should be to define the underlying functional mutations and explore possible disease mechanisms, including the gene-environment interactions that culminate in clinically apparent disease. This review will define a contemporary research paradigm for study of the genetics of CAD and other common chronic diseases using the tools of modern molecular biology and human genetics.
No takes yet. Share an insight, caveat, or question.
Boerwinkle et al. (1996) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: