Welcome to the Molecular Cardiology group
Heart failure, the common end-point in cardiac disease of diverse etiologies, is a major cause of morbidity and mortality in affluent societies. Indeed, the incidence and prevalence of heart failure in these countries are increasing due to altered demographics with increased proportion of the elderly, as well as increased survival of myocardial infarction. Despite implementation of several new treatment modalities during the last 20 years, heart failure is still a progressive and ominous disease indicating that important pathogenic mechanisms remain unmodified by the most current treatment modalities.
Major Aim
Dysfunctional cardiac signaling mechanisms and signals astray are considered major causes of pathologic myocardial hypertrophy and predisposition to heart failure. Dissecting the function of autocrine/paracrine growth factors as well as kinases that regulate signaling cascades may provide important new knowledge as a basis for the development of new and more effective therapeutic intervention in heart failure.
Our research group focuses on two major aims:
- Uncover the function of autocrine/paracrine myocardial mediators that are activated or induced in heart failure. Currently, the focus is on CCN2/CTGF - connective tissue growth factor, a multipotent CCN growth factor that is induced in heart failure of various etiologies.
- Provide novel insights into the function of myocardial G protein-coupled receptor kinases, i.e. a family of kinases that are important proximal modulators of many receptor-controlled signal transduction pathways involved in regulation of myocardial function and growth.
Landscape of cancer genes and mutational processes in breast cancer
May 21, 2012
Latest publications
Håvard Attramadal
Cardiomyocyte-restricted inhibition of G protein-coupled receptor kinase-3 (GRK3) attenuates cardiac dysfunction after chronic pressure overload
Am J Physiol Heart Circ Physiol (in press)
PubMed 22542621
The matri-cellular proteins 'cysteine-rich, angiogenic-inducer, 61' and 'connective tissue growth factor' are regulated in experimentally-induced sepsis with multiple organ dysfunction
Innate Immun (in press)
PubMed 22334618
Lack of chemokine signaling through CXCR5 causes increased mortality, ventricular dilatation and deranged matrix during cardiac pressure overload
PLoS One, 6 (4), e18668
PubMed 21533157
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