Published Online
on February 7, 2005

A more recent version of this article appeared on April 1, 2005

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Submitted on October 7, 2004
Revised on November 15, 2004

Arthur Corcoran Lecture 2004. Cardiovascular Genomics and Oxidative Stress

Anna F. Dominiczak^*; Delyth Graham; Martin W. McBride; Nick J.R. Brain; Wai Kwong Lee; Fadi J. Charchar; Maciej Tomaszewski; Christian Delles; and Carlene A. Hamilton

From the BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Scotland, UK.

^* To whom correspondence should be addressed. E-mail: ad7e{at}clinmed.gla.ac.uk.

Abstract--The majority of modifiable cardiovascular risk factors are complex, polygenic, or at least oligogenic traits, with genetic and environmental determinants playing important roles in disease risk and its phenotypic expression. The Human Genome Project and subsequent mouse and rat genome data have provided powerful tools to commence the dissection of genetic determinants of hypertension and other cardiovascular risk factors. Despite several new methodologies such as genome-wide scans, genome-wide gene expression profiling, and proteomic screens, it is fair to say that the progress of genetic studies designed as nonhypothesis driven has been relatively slow. On the other hand, several interesting candidate pathways have been identified, where investigators allowed for hypothesis-driven functional studies. One example of such pathway is vascular oxidative stress with its extensive network of genes and proteins, many with proven contributions to cardiovascular disease. Therefore, in parallel to genome-wide or proteome-wide studies, it will be constructive to pursue "pathwayomics" defined here as functional studies of a candidate pathway for disease pathogenesis.

Key words: genetics • oxidative stress • endothelium

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