An increasing body of evidence suggests that oxidative stress is involved in the pathogenesis of a wide range of cardiovascular diseases including hypertension, type 2 diabetes, hypercholesterolaemia, atherosclerosis and heart failure. It is a matter for debate whether this increased oxidative stress has a primary causative role in cardiovascular disease pathogenesis or rather is a vascular sequel of disease progression. There is, however, emerging evidence for genetic components from genome-wide gene expression studies and from systematic evaluation of candidate genes within the oxidative stress pathways. In both cases it can be concluded that the restoration of vascular reactive oxygen species to normal is an important but frequently neglected therapeutic target.
04 - 06 Apr 2005
British Endocrine Societies