Stokke group: Translational arrhythmology and electrophysiology

Stokke group

We aim to understand processes that lead to cardiac disease due to pathological electrophysiology, especially arrhythmias. Our goal is that this insight will lead to improved diagnostics and therapy for patients with cardiac disease.

Our translational research team work to unravel fundamental principles of cardiac electrophysiology, in order to provide a better understanding and management of clinical conditions caused by abnormal electrical activity in the heart. We use observations from patients as the outset for our laboratory experiments, and test key findings in large animal models and clinical situations.

 

We want to be able to predict and prevent triggers of arrhythmic events, and to provide a basis for the use of exercise for electrophysiological remodeling in a safe manner. We especially focus on the role of calcium handling by cardiac proteins associated with the sarcoplasmic reticulum, such as RyR2, SERCA2 and CaMKII. To better understand the role of these proteins, we use rodent models of heart failure, CPVT, HCM and ischemia-reperfusion.

 

We combine clinical observations and interventions with molecular biology, cellular electrophysiology, Langendorff-perfused hearts and in vivo characterization by echocardiography, MRI and telemetric ECG recording. We also expose rodent models to exercise training by voluntary running in resistance-controlled running wheels and treadmills. As part of this strategy, we collaborate closely with other research groups with expertise on basic research methods, clinical electrophysiology, cardiac imaging and cardiogenetics. This provides us the opportunity to understand biological processes involved in pathological electrophysiology on a molecular, cellular, organ and organism level.

Group leader Mathis Korseberg Stokke is Professor I at UiO and Consultant Cardiologist at the Arrhythmia Unit, Department of Cardiology, Oslo University Hospital Rikshospitalet. He is also Deputy Director of NORHEART – The Norwegian PhD School of Heart Research. He leads a research group with researchers of different academic backgrounds and specific know-how, from nanotechnology and molecular biology to clinical training in cardiology. The group also collaborates closely with clinicians and researchers at Oslo University Hospital, and with international collaborators in the US, Germany and UK.

 

Group Leader

Mathis Korseberg Stokke

Group Leader & Professor & Senior Consultant

Group members

Kristine Andreassen

Doctoral Research Fellow

Mani Sadredini

Doctoral Research Fellow

Marie Haugsten Hansen

Doctoral Research Fellow

Simon Girmai Berger

Medical Research Curriculum Student

Stine Aagaard-Nilsen

Medical Research Curriculum Student

Tore Kristian Danielsen

Doctoral Research Fellow

Tristan Hellstrand

Medical Research Curriculum Student

Latest publications

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Andreassen K, Dejgaard LA, Lie Ø, Fink TS, Lunde IG, Edvardsen T, Haugaa KH, Stokke MK (2022)
Exercise training during childhood and adolescence is associated with favorable diastolic function in hypertrophic cardiomyopathy
Int J Cardiol, 364, 65-71
PubMed 35714718 DOI 10.1016/j.ijcard.2022.06.042
Harbo MB, Stokke MK, Sjaastad I, Espe EKS (2022)
One step closer to myocardial physiology: From PV loop analysis to state-of-the-art myocardial imaging
Acta Physiol (Oxf), 234 (2), e13759
PubMed 34978759 DOI 10.1111/apha.13759
Edwards AG, Mørk H, Stokke MK, Lipsett DB, Sjaastad I, Richard S, Sejersted OM, Louch WE (2021)
Sarcoplasmic Reticulum Calcium Release Is Required for Arrhythmogenesis in the Mouse
Front Physiol, 12, 744730
PubMed 34712150 DOI 10.3389/fphys.2021.744730
Sadredini M, Manotheepan R, Lehnart SE, Anderson ME, Sjaastad I, Stokke MK (2021)
The oxidation-resistant CaMKII-MM281/282VV mutation does not prevent arrhythmias in CPVT1
Physiol Rep, 9 (18), e15030
PubMed 34558218 DOI 10.14814/phy2.15030
Sadredini M, Haugsten Hansen M, Frisk M, Louch WE, Lehnart SE, Sjaastad I, Stokke MK (2021)
CaMKII inhibition has dual effects on spontaneous Ca2+ release and Ca2+ alternans in ventricular cardiomyocytes from mice with a gain-of-function RyR2 mutation
Am J Physiol Heart Circ Physiol, 321 (2), H446-H460
PubMed 34270372 DOI 10.1152/ajpheart.00011.2021
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