Compromised repolarization reserve in a murine model of catecholaminergic polymorphic ventricular tachycardia caused by RyR2-R420Q mutation
Ca<sup>2+</sup>-mediated AP lengthening and EADs may contribute to proarrhythmic behaviour in CPVT caused by gain-of-function R420Q mutation. Loss of repolarization reserve is not specifically targeted by CPVT therapies but could be an opportunity for therapeutic intervention.
Authors
- Ewan D. Fowler (ORCID: https://orcid.org/0000-0001-5580-2156)
- Esther Zorio (ORCID: https://orcid.org/0000-0003-3608-4210)
- Yueyi Wang (ORCID: https://orcid.org/0000-0001-8613-2239)
- Spyros Zissimopoulos (ORCID: https://orcid.org/0000-0001-5196-9450)
- Branko Latinkic (ORCID: https://orcid.org/0000-0003-4952-123X)
- Aitana Braza‐Boïls (ORCID: https://orcid.org/0000-0002-9888-6705)
- Mark B. Cannell (ORCID: https://orcid.org/0000-0002-4816-0463)
- Ana M. Gómez (ORCID: https://orcid.org/0000-0003-0009-2884)
- Pavel Kirilenko
Institutions
- University of Bristol (GB)
- Swansea University (GB)
- Cardiff University (GB)
Publication Details
- Journal
- Journal of Molecular and Cellular Cardiology
- Published
- 2025-07-24
- DOI
- https://doi.org/10.1016/j.yjmcc.2025.07.014
- Citations
- 2
- Primary Topic
- Cardiac electrophysiology and arrhythmias
- Type
- article
- Field-Weighted Citation Impact
- 2.78
Funders
- British Heart Foundation
- Cardiff University
- Agence Nationale de la Recherche
- China Scholarship Council
- Fundación Bancaja
- National Institutes of Health
- Medical Research Council
- CHIST-ERA