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Krause, J.* ; Nickel, A.* ; Madsen, A.* ; Aitken-Buck, H.M.* ; Stoter, A.M.S.* ; Schrapers, J.* ; Ojeda, F.* ; Geiger, K.* ; Kern, M.* ; Kohlhaas, M.* ; Bertero, E.* ; Hofmockel, P.* ; Hübner, F.* ; Assum, I. ; Heinig, M. ; Müller, C.* ; Hansen, A.* ; Krause, T.* ; Park, D.D.* ; Just, S.* ; Aïssi, D.* ; Börnigen, D.* ; Lindner, D.* ; Friedrich, N.* ; Alhussini, K.* ; Bening, C.* ; Schnabel, R.B.* ; Karakas, M.* ; Iacoviello, L.* ; Salomaa, V.* ; Linneberg, A.* ; Tunstall-Pedoe, H.* ; Kuulasmaa, K.* ; Kirchhof, P.* ; Blankenberg, S.* ; Christ, T.* ; Eschenhagen, T.* ; Lamberts, R.R.* ; Maack, C.* ; Stenzig, J.* ; Zeller, T.*

An arrhythmogenic metabolite in atrial fibrillation.

J. Transl. Med. 21:566 (2023)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
BACKGROUND: Long-chain acyl-carnitines (ACs) are potential arrhythmogenic metabolites. Their role in atrial fibrillation (AF) remains incompletely understood. Using a systems medicine approach, we assessed the contribution of C18:1AC to AF by analysing its in vitro effects on cardiac electrophysiology and metabolism, and translated our findings into the human setting. METHODS AND RESULTS: Human iPSC-derived engineered heart tissue was exposed to C18:1AC. A biphasic effect on contractile force was observed: short exposure enhanced contractile force, but elicited spontaneous contractions and impaired Ca2+ handling. Continuous exposure provoked an impairment of contractile force. In human atrial mitochondria from AF individuals, C18:1AC inhibited respiration. In a population-based cohort as well as a cohort of patients, high C18:1AC serum concentrations were associated with the incidence and prevalence of AF. CONCLUSION: Our data provide evidence for an arrhythmogenic potential of the metabolite C18:1AC. The metabolite interferes with mitochondrial metabolism, thereby contributing to contractile dysfunction and shows predictive potential as novel circulating biomarker for risk of AF.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Acyl-carnitine ; Atrial Fibrillation ; Engineered Heart Tissue ; Metabolites ; Translational Medicine; Long-chain Acylcarnitines; Fatty-acid Oxidation; Heart; Mitochondrial; Calcium; Cardiomyocytes; Myocardium; Tissue; Leak
Sprache englisch
Veröffentlichungsjahr 2023
HGF-Berichtsjahr 2023
ISSN (print) / ISBN 1479-5876
e-ISSN 1479-5876
Zeitschrift Journal of Translational Medicine
Quellenangaben Band: 21, Heft: 1, Seiten: , Artikelnummer: 566 Supplement: ,
Verlag BioMed Central
Verlagsort Campus, 4 Crinan St, London N1 9xw, England
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Computational Biology (ICB)
POF Topic(s) 30205 - Bioengineering and Digital Health
Forschungsfeld(er) Enabling and Novel Technologies
PSP-Element(e) G-554700-001
G-553500-001
Förderungen German Research Foundation (DFG)
Federal Ministry of Education and Research (BMBF)
German Center for Cardiovascular Research (DZHK)
Project DEAL
BiomarCaRE/MORGAM (European Commission)
ERA-CVD PREMED-CAD (European Research Area Network on Cardiovascular Diseases Precision Medicine in Coronary Artery Disease)
DZHK
Finnish Foundation for Cardiovascular Research
Juho Vainio Foundation
Barth Syndrome Foundation
Heart Foundation of New Zealand
European Research Council
European Research Council (ERC) under the European Union
European Union
ERACoSysMed3
DOI 10.1186/s12967-023-04420-z
WOS ID 001055365900003
Scopus ID 85168691763
PubMed ID 37620858
Erfassungsdatum 2023-10-06
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