MINI-SYMPOSIUM

Free radicals and redox signalling in cardiovascular disease

A M Shah¹, K M Channon²

¹ Department of Cardiology, Guy’s King’s & St Thomas’s School of Medicine, King’s College London, UK
² Department of Cardiovascular Medicine, University of Oxford, UK

Correspondence to:
Correspondence to:
Professor A M Shah
Department of Cardiology, GKT School of Medicine, Bessemer Road, London SE5 9PJ, UK; ajay.shah{at}kcl.ac.uk

Keywords: free radicals; redox signalling; gene expression; cardiovascular disease

Abbreviations: MAPKs, mitogen activated protein kinases; NO, nitric oxide; NOS, nitric oxide synthases; ROS, reactive oxygen species; SOXF, secreted oxidative stress induced factors

The first 150 words of the full text of this article appear below.

The generation of reactive oxygen species (ROS) is an inevitable consequence of life in an aerobic environment. ROS are characterised by their high chemical reactivity and include both free radicals (that is, species with one or more unpaired electrons, such as superoxide (O₂^.−) and hydroxyl radicals (OH^.)), and non-radical species such as hydrogen peroxide (H₂O₂). In health, there is a balance between ROS generation and the activity of enzymatic and non-enzymatic antioxidant systems that scavenge or reduce ROS concentrations.¹ Redox imbalance caused by increased ROS production and/or reduced antioxidant reserve causes oxidative stress—that is, an enhanced susceptibility of biological molecules and membranes to reaction with ROS.

Traditionally, oxidative stress has been considered deleterious due to free radical induced oxidation and damage of macromolecules, membranes and DNA. ROS generation by phagocytic cells such as neutrophils is a pivotal component of their antimicrobial actions and as such deleterious . . . [Full text of this article]

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