Department of Cardiology, Oslo University Hospital Ullevaal and Institute for Experimental Medical Research, Oslo University Hospital Ullevaal

Current research focus

• Regulation of excitation-contraction coupling.
• In vivo cardiac function.

Research projects

Supervisor

• Electrical remodelling in heart failure
• SERCA2-RyR2 interplay underlying triggered arrhythmias
• Exercise and heart failure in patients
• Targeting of Na⁺ transporting proteins determines cardiac contractility and rhythm
• Heart failure protein interaction
• L-type Ca2+ current inhibition for prevention of triggered arrhythmias
• Exercise training as anti-arrhythmic therapy in heart failure
• Mechanisms regulating left ventricular remodelling in patients with aortic stenosis.
• Skeletal muscle fatigue mechanisms in rats and humans
• Optimization of gene deletion protocols in mouse models utilizing Mer-Cre-Mer (MCM) technology
• Phosphodiesterase regulation of SERCA2 activity

Collaborator

• Hematopoiesis in mice with heart failure
• Regulation of serotonin receptor expression in normal and failing hearts
• Changes of adrenergic receptor functions in failing myocardium
• Involvement of phosphorylation of myosin light chain (MLC) in the inotropic responses to stimulation of Gq coupled receptors
• Mechanism of action of 5-HT₄ serotonin receptors in failing myocardium
• Skeletal muscle fatigue during heart failure in rats
• Exercise and heart failure in patients
• The connection between membrane potential and contractility is changed in heart failure
• Modelling of excitation-contraction coupling
• Calcium homeostasis and the failing heart
• Mechanisms underlying the force-frequency response in normal and failing cardiomyocytes
• The importance of skeletal muscle extracellular matrix in CHF related fatigue and the role of skeletal muscle in the systemic inflammatory state of heart failure
• A comparison between the receptor signalling mechanisms coupled to 5-HT4 serotonin receptors and to beta-adrenoceptors in failing myocardium.
• Crosstalk of cGMP on cAMP signalling systems in cardiomyocytes. A key to modifications of cAMP-dependent receptor functions in failing myocardium?
• Characterization of increased calcium sensitivity in heart muscle as inotropic mechanism for receptor stimulation and for levosimendan.
• Effects and mechanisms of muscarinic receptor stimulation in failing myocardium
• Chromogranin A, granins and heart disease
• Identification and modulation of signaling complexes involved in hypertrophy and heart failure
• Regulation of myocardial cGMP by PDE subtypes.
• New aspects in myocardial remodeling and dysfunction due to left ventricular pressure overload
• The homeostatic chemokine CXCL13 and its receptor CXCR5 are regulated in experimental and human heart failure, and are involved in cardiac remodelling.
• Role of inflammatory mediators in right ventricular pressure overload
• Signalling mechanisms for the negative inotropic effect of natriuretic peptides in failing myocardium
• The role of interleukin-18 in cardiac hypertrophy and heart failure
• 3D imaging of the dyad
• IP₃ signalling and Ca²⁺-wave development in ventricular cardiomyocytes
• Spatial homogeneity of cardiomyocyte Ca²⁺ handling and sarcomeric function
• The role of syndecan-4 in extracellular matrix remodeling in response to pressure overload
• The role of collagen type VIII during reverse myocardial remodelling
• Role of Neil3 in regulating stem cell recruitment following myocardial infarction
• Crosstalk between transport proteins that control intracellular sodium in cardiomyoctyes
• cGMPs influence on cAMP
• Small leucine rich proteoglycans and reverse remodelling of cardiac extracellular matrix