Transgenic short-QT syndrome 1 rabbits mimic the human disease phenotype with QT/action potential duration shortening in the atria and ventricles and increased ventricular tachycardia/ventricular fibrillation inducibility

Autor: David Ziupa, Heiko Bugger, Anna Ryan de Medeiros, Marius Menza, Corinna N. Lang, Stefanie Perez-Feliz, Jan C. Behrends, Michael Brunner, Naga Deepa Pantulu, Lea Mettke, Konstantin Michaelides, Zoltán Doleschall, Raphaela Rieke, Rémi Peyronnet, Geneviève Jolivet, Christoph Bode, Axel zur Hausen, Hannah E Fürniss, Ilona Bodi, Manfred Zehender, Katja E. Odening, Johannes Steinfurt, Gerlind Franke

Publikováno v: European Heart Journal
European Heart Journal, Oxford University Press (OUP): Policy B, 2019, 40 (10), pp.842-853. ⟨10.1093/eurheartj/ehy761⟩
European Heart Journal, 40(10), 842-853. Oxford University Press

AIMS Short-QT syndrome 1 (SQT1) is an inherited channelopathy with accelerated repolarization due to gain-of-function in HERG/IKr. Patients develop atrial fibrillation, ventricular tachycardia (VT), and sudden cardiac death with pronounced inter-indi

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c11c471e972d6411e8038719e68b7b5c
https://hal.inrae.fr/hal-02619630