This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Wolin, M. S. Articles by Gupte, S. A. Search for Related Content PubMed PubMed Citation Articles by Wolin, M. S. Articles by Gupte, S. A. Related Collections Arrythmias-basic studies Oxidant stress Endothelium/vascular type/nitric oxide Related Articles

(Circulation Research. 2005;97:612.)
© 2005 American Heart Association, Inc.

Editorials

Novel Roles for Nox Oxidases in Cardiac Arrhythmia and Oxidized Glutathione Export in Endothelial Function

Michael S. Wolin, Sachin A. Gupte

From the Department of Physiology, New York Medical College, Valhalla, NY.

Correspondence to Michael S. Wolin, Department of Physiology, Basic Sciences Bldg, Rm 604, New York Medical College, Valhalla, NY 10595. E-mail mike_wolin@nymc.edu

See related articles, pages 629–636 and pages 637–644

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
This issue of Circulation Research contains two articles in the area of oxidant regulation that have major implications for their novel roles in mechanisms that contribute to cardiovascular disease processes in humans. An article by Kim et al¹ reports data showing that human cardiac myocytes isolated from right atrial appendages express Nox-2, and that these myocytes and homogenates of the atria from patients with atrial fibrillation (AF) have increased levels of Nox-derived superoxide generation that appear to originate from increased Nox oxidase activation. Homogenates of atria from the AF patients also show evidence of nitric oxide synthase (NOS) becoming a source of superoxide generation, which is thought to originate from an uncoupling of the ability of this enzyme to efficiently synthesize NO. The article by Mueller et al² reports a new important role for multidrug resistance protein-1 (MRP-1) in controlling oxidant regulation in human and animal endothelium by exporting oxidized glutathione (GSSG). In their study, this group demonstrates how the expression of this protein functions to remove increased GSSG in hypertensive rats and endothelial cells exposed to oscillatory shear stress. Interestingly, the inhibition of MRP-1 appears to restore endothelial function in the hypertensive rats and prevent shear-induced apoptosis in these models apparently through preserving endothelial cell glutathione levels. Both of these articles have major new implications for the understanding and therapeutic targeting of human disease processes.

	Nox Oxidases in Cardiac Arrhythmia

 
There is already much evidence that oxidant processes have a major influence on the expression of AF. As discussed in the article by Kim . . . [Full Text of this Article]

Related Articles:

The Role of the Multidrug Resistance Protein-1 in Modulation of Endothelial Cell Oxidative Stress

Cornelius F.H. Mueller, Julian D. Widder, Joseph S. McNally, Louise McCann, Dean P. Jones, and David G. Harrison
Circ. Res. 2005 97: 637-644. [Abstract] [Full Text] [PDF]

A Myocardial Nox2 Containing NAD(P)H Oxidase Contributes to Oxidative Stress in Human Atrial Fibrillation

Young M. Kim, Tomasz J. Guzik, Yin Hua Zhang, Mei Hua Zhang, Hassan Kattach, Chandi Ratnatunga, Ravi Pillai, Keith M. Channon, and Barbara Casadei
Circ. Res. 2005 97: 629-636. [Abstract] [Full Text] [PDF]