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Cardiovascular Research Advance Access [Accepted Manuscript] published online on March 7, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn060
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Heat Shock Proteins as Molecular Targets for Intervention in Atrial Fibrillation

Bianca J.J.M. Brundel1,2,, Lei Ke1, Anne-Jan Dijkhuis1, XiaoYan Qi3, Akiko Shiroshita-Takeshita3,4, Stanley Nattel3, Robert H. Henning2 and Harm H. Kampinga1

1 Department of Radiation and Stress Cell Biology, University Groningen, University Medical Center Groningen, The Netherlands
2 Department of Clinical Pharmacology, University Groningen, University Medical Center Groningen, The Netherlands
3 Department of Medicine and Research Center, Montreal Heart Institute and Université de Montréal, Canada, and Keio University School of Medicine, Tokyo, Japan
4 Department of Emergency and Critical Care Medicine, Keio University School of Medicine, Tokyo, Japan

Address correspondence to: Bianca Brundel, Department of Radiation and Stress Cell Biology, University of Groningen, UMCG, A. Deusinglaan 1, 9713 AV Groningen, The Netherlands. Tel.: 31 50 3633399; Fax: 31 50 3632913; E-mail: B.J.J.M.Brundel{at}med.umcg.nl

Atrial Fibrillation (AF) is the most common sustained clinical tachyarrhythmia. AF is a progressive condition as demonstrated by the finding that maintenance of normal rhythm and contractile function becomes more difficult the longer AF exists. AF causes cellular stress, which induces atrial remodeling, involving reduction in the expression of L-type Ca2+ channels and structural changes (myolysis), finally resulting in contractile dysfunction. Heat shock proteins (HSPs) comprise a family of proteins involved in the protection against different forms of cellular stress. Their classical function is the prevention of toxic protein aggregation by binding to (partially) unfolded proteins. Recent investigations reveal that HSPs prevent atrial remodeling and attenuate the promotion of AF in both cellular and animal experimental models. Furthermore, studies in humans suggest a protective role for HSPs against progression from paroxysmal AF to chronic, persistent AF. Therefore, manipulation of the HSP system may offer novel therapeutic approaches for the prevention of atrial remodeling. Such approaches may contribute to the maintenance or restoration of tissue integrity and contractile function. Ultimately, this concept may offer an additional treatment strategy to delay progression towards chronic AF and/or improve the outcome of cardioversion.

Time for primary review: 19 days


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