Institute for Surgical Research, Oslo University Hospital Rikshospitalet

Current research focus

The major focus of the research group is on the pathophysiologic mechanisms of myocardial hypertrophy and heart failure. In particular the research group is working to resolve signaling signaling mechanisms involved in cardioprotection versus progression of heart failure. The group is currently investigating the matricellular protein CCN2/CTGF and its signaling pathways in cardiac myocytes and fibroblasts, and the functions of the various myocardial G protein-coupled receptor kinase isoforms (GRKs).

Research projects

Supervisor

• Significance of pulmonary monocyte/macrophage system in the pathophysiologic mechanisms of heart failure
• Substrate specificities and function of G protein-coupled receptor kinase (GRK) isoforms in adult, differentiated cardiac myocytes
• Involvement of GRK3 in the pathophysiologic mechanisms of heart failure
• Mechanisms of elevated plasma endothelin-1 levels in heart failure
• Functional significance of CTGF-induced restrictive fibrosis of the heart in endurance training vs. heart failure
• Role of myocardial CTGF in the pathophysiologic mechanisms of heart failure
• Functions of myocardial CTGF in the postnatal heart – signalling pathways, delineation of CTGF-induced gene expression programs and role in cell proliferation, differentiation and cell death
• Mechanisms of myocardial CTGF-induced arrythmias
• Identification and characterization of factors that stimulate proliferation and survival of cardiac stem cells
• Mechanisms of cardioprotection
• Identification of factors that stimulate survival and proliferation of cardiac progenitor cells.
• Investigation of role of G protein receptor kinase-5 (GRK5) in cardioprotection
• Generation of transgenic mice with inducible, cardiac-restricted expression of CTGF
• Characterization of intracellular signaling pathways of CTGF and mechanisms of cytoprotective actions in cardiac myocytes
• Role of CCN2/CTGF in in autonomic control of the heart

Collaborator

• Hematopoiesis in mice with heart failure
• The role of fetal gene programs for development of acute infarction and postischemic heart failure
• Is heme oxygenase-1 a downstream mediator of HIF-1a induced protection?
• Mitochondrial p66Shc - fiend or foe?
• Mechanisms regulating reverse remodeling after relief of pressure overload of the left ventricle
• The homeostatic chemokine CXCL13 and its receptor CXCR5 are regulated in experimental and human heart failure, and are involved in cardiac remodelling.
• Role of the innate immun system in the development and maintenance of cardiovascular disease
• A role of retinoic acid in remodelling of the failing heart
• Gender and cardiovascular disease
• Pathophysiological role of inflammatory cytokines in heart failure