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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 article by Jin and Berk addressing recently identified novel redox signalling mechanisms. Kathy Griendling reviews the fascinating family of enzymes known as NADPH oxidases, which have recently been identified as major players in redox signalling in several cardiovascular disorders. Finally, Verhaar and colleagues discuss the potential pathogenic importance of superoxide production by NOS, the enzyme that normally generates NO but can switch to ROS production when the NOS co-factor tetrahydrobiopterin is deficient—for example, in diabetic vasculopathy. We hope that this mini-symposium will provide an up-to-date review of the important field of oxidative stress and redox signalling and its relevance to clinical cardiovascular disease.
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