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(Circulation Research. 2005;96:923.)
© 2005 American Heart Association, Inc.

Editorials

Ventricularization of Atrial Gene Expression in the Fibrillating Heart?

Gordon F. Tomaselli

From the Johns Hopkins University School of Medicine, Donald W. Reynolds Clinical Cardiovascular Research Center, Baltimore, Md.

Correspondence to Gordon F. Tomaselli, MD, Professor of Medicine, Vice-Chair for Research, DOM, John Hopkins University School of Medicine, 720 Rutland Avenue/Ross 844, Baltimore, MD 21205. E-mail gtomasel@jhmi.edu

See related article, pages 1022–1029

Key Words: atrial fibrillation • microarray • RNA • arrhythmia • potassium channels • calcium handling • metabolism • transcription

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

Structural and functional changes in the heart in response to disease or dysfunction are essential compensatory responses to stress. In the context of sustained stress such initially adaptive changes may become maladaptive or contribute to the progression of the pathological phenotype. Understanding the cellular and molecular basis of such remodeling holds the promise of understanding disease mechanisms and identifying novel therapeutic targets and interventions.

Atrial fibrillation (AF) is the most common sustained arrhythmia in man and has justifiably been an area in which remodeling has been intensely investigated. The atria undergo a complex, time dependent series of changes in structure and cellular electrophysiological function in response to rapid atrial activation and heart disease that predispose the development of AF. Canonical individual gene and pathway, transcriptional, translational, and functional studies of animal model and human AF have identified changes in a number of important regulatory pathways in the fibrillating atria that have helped to explain the self-perpetuation of this arrhythmia or why "AF begets more AF". In this sense, some of the findings of Barth et al¹ benefits from this "cart before the horse sequence of events" and indeed validates some of the findings in the microarray dataset. That is, some of the transcriptomal changes in permanent AF identified by microarray analysis have previously been demonstrated in AF. In particular changes in ionic current expression,^2,3 Ca handling, and profibrotic signaling are consistent with published structural and functional data (for review see^4,5). Cross platform consistency, suggests the importance of such changes . . . [Full Text of this Article]

Related Article:

Reprogramming of the Human Atrial Transcriptome in Permanent Atrial Fibrillation: Expression of a Ventricular-Like Genomic Signature

Andreas S. Barth, Sylvia Merk, Elisabeth Arnoldi, Ludwig Zwermann, Patrick Kloos, Mathias Gebauer, Klaus Steinmeyer, Markus Bleich, Stefan Kääb, Martin Hinterseer, Heike Kartmann, Eckart Kreuzer, Martin Dugas, Gerhard Steinbeck, and Michael Nabauer
Circ. Res. 2005 96: 1022-1029. [Abstract] [Full Text] [PDF]

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