Format

Send to

Choose Destination
J Mol Cell Cardiol. 2013 Sep;62:72-9. doi: 10.1016/j.yjmcc.2013.04.019. Epub 2013 May 2.

Oxidative stress in atrial fibrillation: an emerging role of NADPH oxidase.

Author information

1
Divisions of Molecular Medicine and Cardiology, Department of Anesthesiology, Cardiovascular Research Laboratory (CVRL), David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA, USA.

Abstract

Atrial fibrillation (AF) is the most common cardiac arrhythmia. Patients with AF have up to seven-fold higher risk of suffering from ischemic stroke. Better understanding of etiologies of AF and its thromboembolic complications are required for improved patient care, as current anti-arrhythmic therapies have limited efficacy and off target effects. Accumulating evidence has implicated a potential role of oxidative stress in the pathogenesis of AF. Excessive production of reactive oxygen species (ROS) is likely involved in the structural and electrical remodeling of the heart, contributing to fibrosis and thrombosis. In particular, NADPH oxidase (NOX) has emerged as a potential enzymatic source for ROS production in AF based on growing evidence from clinical and animal studies. Indeed, NOX can be activated by known upstream triggers of AF such as angiotensin II and atrial stretch. In addition, treatments such as statins, antioxidants, ACEI or AT1RB have been shown to prevent post-operative AF; among which ACEI/AT1RB and statins can attenuate NOX activity. On the other hand, detailed molecular mechanisms by which specific NOX isoform(s) are involved in the pathogenesis of AF and the extent to which activation of NOX plays a causal role in AF development remains to be determined. The current review discusses causes and consequences of oxidative stress in AF with a special focus on the emerging role of NOX pathways.

KEYWORDS:

Atrial fibrillation; NADPH oxidase; NOX2; NOX4; Oxidative stress; Structural and electrical remodeling

PMID:
23643589
PMCID:
PMC3735724
DOI:
10.1016/j.yjmcc.2013.04.019
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center