| Literature DB >> 31118294 |
Katharina Scherschel1,2, Katja Hedenus1,2, Christiane Jungen1,2, Marc D Lemoine1,2,3, Nicole Rübsamen4, Marieke W Veldkamp5, Niklas Klatt1,2, Diana Lindner2,4, Dirk Westermann2,4, Simona Casini5, Pawel Kuklik1,2, Christian Eickholt1,2, Nikolaj Klöcker6, Kalyanam Shivkumar7, Torsten Christ2,3, Tanja Zeller2,4, Stephan Willems1,2, Christian Meyer8,2.
Abstract
Atrial fibrillation (AF), the most common sustained heart rhythm disorder worldwide, is linked to dysfunction of the intrinsic cardiac autonomic nervous system (ICNS). The role of ICNS damage occurring during catheter-based treatment of AF, which is the therapy of choice for many patients, remains controversial. We show here that the neuronal injury marker S100B is expressed in cardiac glia throughout the ICNS and is released specifically upon catheter ablation of AF. Patients with higher S100B release were more likely to be AF free during follow-up. Subsequent in vitro studies revealed that murine intracardiac neurons react to S100B with diminished action potential firing and increased neurite growth. This suggests that release of S100B from cardiac glia upon catheter-based treatment of AF is a hallmark of acute neural damage that contributes to nerve sprouting and can be used to assess ICNS damage.Entities:
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Year: 2019 PMID： 31118294 DOI： 10.1126/scitranslmed.aav7770
Source DB: PubMed Journal: Sci Transl Med ISSN： 1946-6234 Impact factor: 17.956