Cardiac glial cells release neurotrophic S100B upon catheter-based treatment of atrial fibrillation

Author:

Scherschel Katharina12ORCID,Hedenus Katja12ORCID,Jungen Christiane12ORCID,Lemoine Marc D.123ORCID,Rübsamen Nicole4ORCID,Veldkamp Marieke W.5ORCID,Klatt Niklas12,Lindner Diana24ORCID,Westermann Dirk24,Casini Simona5,Kuklik Pawel12,Eickholt Christian12ORCID,Klöcker Nikolaj6,Shivkumar Kalyanam7ORCID,Christ Torsten23ORCID,Zeller Tanja24,Willems Stephan12,Meyer Christian12ORCID

Affiliation:

1. Department of Cardiology-Electrophysiology, cNEP (cardiac Neuro- and Electrophysiology research group), University Heart Centre, University Hospital Hamburg-Eppendorf, 20246 Hamburg, Germany.

2. DZHK (German Centre for Cardiovascular Research), partner site Hamburg/Kiel/Lübeck, 13347 Berlin, Germany.

3. Institute of Experimental Pharmacology and Toxicology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.

4. Department of General and Interventional Cardiology, University Heart Center Hamburg, University Hospital Hamburg-Eppendorf, 20246 Hamburg, Germany.

5. Department of Clinical and Experimental Cardiology, Heart Center, Academic Medical Center, 1105 AZ, Amsterdam, Netherlands.

6. Institute of Neural and Sensory Physiology, Medical Faculty, University of Düsseldorf, 40225 Düsseldorf, Germany.

7. Cardiac Arrhythmia Center and Neurocardiology Research Center of Excellence, Molecular, Cellular and Integrative Physiology Interdepartmental Program, UCLA, Los Angeles, CA 90095, USA.

Abstract

Catheter ablation for atrial fibrillation induces intracardiac neural damage characterized by glial S100B release, which promotes nerve sprouting.

Funder

NIH Office of the Director

Deutsches Zentrum für Herz-Kreislaufforschung

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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