Trends in Cardiovascular Medicine
Volume 16, Issue 1 , Pages 20-24, January 2006

β1-Adrenergic Receptor Function, Autoimmunity, and Pathogenesis of Dilated Cardiomyopathy

  • Roland Jahns

      Affiliations

    • Corresponding Author InformationAddress correspondence to: Roland Jahns, MD, Medizinische Klinik und Poliklinik I, University of Würzburg, Josef-Schneider-Strasse 2, D-97080 Würzburg, Germany. Tel.: +49-931-201-71190; fax: +49-931-201-70730.
  • ,
  • Valérie Boivin
  • ,
  • Martin J. Lohse

Department of Internal Medicine, Medizinische Klinik und Poliklinik I, University of Würzburg, D-97080 Würzburg, Germany

Institute of Pharmacology and Toxicology, University of Würzburg, D-97078 Würzburg, Germany

Dilated cardiomyopathy (DCM) is a heart disease characterized by progressive depression of cardiac function and left ventricular dilatation of unknown etiology in the absence of coronary artery disease. Genetic causes and cardiotoxic substances account for about one third of the DCM cases, but the etiology of the remaining 60% to 70% is still unclear. Over the past two decades, evidence has accumulated continuously that functionally active antibodies or autoantibodies targeting cardiac β1-adrenergic receptors (anti-β1-AR antibodies) may play an important role in the initiation and/or clinical course of DCM. Recent experiments in rats indicate that such antibodies can actually cause DCM. This article reviews current knowledge and recent experimental and clinical findings focusing on the role of the β1-adrenergic receptor as a self-antigen in the pathogenesis of DCM.

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PII: S1050-1738(05)00216-1

doi:10.1016/j.tcm.2005.11.002

Trends in Cardiovascular Medicine
Volume 16, Issue 1 , Pages 20-24, January 2006