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Heart 2004;90:485; doi:10.1136/hrt.2003.032482
Copyright © 2004 BMJ Publishing Group Ltd & British Cardiovascular Society
Heart 2004;90:485
© 2004 by BMJ Publishing Group & British Cardiac Society

MINI-SYMPOSIUM

Free radicals and redox signalling in cardiovascular disease: introduction

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; ajay.shah{at}kcl.ac.uk
2 Department of Cardiovascular Medicine, University of Oxford, UK

Keywords: free radicals; redox signalling; reactive oxygen species

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

Reactive oxygen species (ROS) are highly reactive chemical species comprising both free radicals such as superoxide and non-radicals such as hydrogen peroxide. When the normal balance between ROS generation and antioxidant systems is perturbed, a state of oxidative stress is said to exist, which has traditionally been considered deleterious due to tissue oxidation and damage. Recently, however, ROS have been recognised to exert more subtle effects. Tightly regulated ROS production modulates intracellular signalling pathways ("redox signalling") and can induce highly specific changes in cell phenotype, especially in pathological settings. ROS also inactivate the signalling molecule nitric oxide (NO) and cause endothelial dysfunction, which may itself be a contributor to disease pathogenesis.

The following articles in this mini-symposium address several topical aspects of the roles of ROS in cardiovascular disease. The overview article by Shah and Channon considers general mechanisms, effects, and relevance of redox signalling, and is followed by an . . . [Full text of this article]


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