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RADical reduction of OXidative stress in cardiovascular diseases

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Oxidative stress in cardiovascular disease

Cardiovascular disease (CVD) constitutes a major health burden in developed countries with a predicted increase in prevalence over the next 20 years. Comprehending the causes of CVD pathophysiology is central to the design of effective interventions.

Fundamental Research
Health

Oxidative stress is an important molecular contributor to the pathogenesis of CVD. Excessive production of reactive oxygen species (ROS) causes cell senescence, affects the vasculature by causing endothelial dysfunction and supports atherosclerosis through the release of metalloproteases. Various risk factors related to lifestyle or ageing may impair resistance to cellular oxidative stress, thereby contributing to CVD development. The EU-funded RADOX project wished to characterise the specific sources of ROS and their interaction in CVD. The goal being to use this knowledge to develop diagnostic tools for the detection and quantification of ROS and their subcellular targets. The consortium combined expertise from nine different institutes across Europe who provided multidisciplinary scientific and transferable skills training to young researchers. The rationale was to create the next generation of researchers who will further research oxidative stress and CVDs. From a scientific perspective, the recruited researchers worked on arrhythmia, myocardial pathophysiology and therapeutics, while others focused more on vascular development and hypertension. Additional projects included research on protection from ROS-induced cardiac injury. Significant achievements were made in the identification of ROS sources and their molecular targets, offering a new angle in CVD pathophysiology. In addition, to be able to diagnose increased ROS levels in humans, researchers discovered biomarkers and genetic targets that allowed quantification of oxidative stress in cell culture systems and animal models. This data was also used as a means of predicting risk for increased ROS generation in humans. Furthermore, to prevent or reverse the molecular damage caused by oxidative stress, the consortium examined the inhibition of specific sources of ROS as a treatment. Overall, the knowledge generated during RADOX advances the field of cardiovascular research and supports the development of new therapeutic strategies, which modulate the activity of these specific sources of ROS.

Keywords

Oxidative stress, cardiovascular disease, ROS, RADOX, biomarker

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