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beta(2)-Adrenoceptors, NADPH oxidase, ROS and p38 MAPK: another 'radical' road to heart failure? (Articolo in rivista)

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beta(2)-Adrenoceptors, NADPH oxidase, ROS and p38 MAPK: another 'radical' road to heart failure? (Articolo in rivista) (literal)

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Di Lisa, Fabio; Kaludercic, Nina; Paolocci, Nazareno (2011)
beta(2)-Adrenoceptors, NADPH oxidase, ROS and p38 MAPK: another 'radical' road to heart failure?
in British journal of pharmacology
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1: Department of Biomedical Sciences, University of Padova, Padova, Italy / Institute for Neuroscience, CNR, Padova, Italy; 2: Department of Biomedical Sciences, University of Padova, Padova, Italy; 3: Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA / Department of Clinical Medicine, Section of General Pathology, University of Perugia, Perugia, Italy (literal)

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beta(2)-Adrenoceptors, NADPH oxidase, ROS and p38 MAPK: another 'radical' road to heart failure? (literal)

Abstract

Persistent activation of the cardiac b-adrenergic system may contribute to the pathogenesis of congestive heart failure. Both b1- and b2-adrenoceptors are known to mediate these noxious effects, yet the b1-adrenoceptor-PKA axis has received greater attention with less information available on b2-adrenoceptor driven pathways. In the present issue, Xu and colleagues provide new evidence, showing that b2-adrenoceptor over-expression leads to increased reactive oxygen species (ROS) emission, mainly caused by up-regulation of reduced nicotinamide adenine dinucleotide phosphate oxidase (Nox) 2 and 4. Increase in ROS levels is accompanied by p38 mitogen-activated protein kinase activation, fibrosis, apoptosis and cardiac dysfunction. Both Nox inhibition and administration of the antioxidant N-acetyl cysteine prevent these adverse effects. Interestingly, antioxidant treatment also prevents the increase in Nox expression, suggesting that b2-adrenoceptor stimulation triggers a vicious cycle eventually amplified by both Nox isoforms. The possible existence of a circuitry to enhance ROS signalling and detrimental consequences on myocardial remodelling are also discussed, in light of the recent description of intracellular localization of Nox4. (literal)
This article is a commentary on Xu et al., pp. 1012-1028 of this issue. To view this paper visit http://dx.doi.org/10.1111/j.1476-5381.2010.01043.x. (literal)

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