Lipoprotein and atherosclerosis research
The overall theme of our research is basic and clinical aspects of atherosclerosis and how disturbances in the lipid/lipoprotein metabolism affect cardiovascular disease.
We work in research laboratory facilities at the Department of Clinical Biochemistry, Rigshospitalet and Department of Biomedical Sciences, University of Copenhagen and collaborate with groups at Rigshospitalet, KU, Aarhus, Sweden, USA, New Zealand, Holland, Germany, Finland, and Austria.
Our major research project lines
Apolipoproteins (apo's) are plasma proteins associated with lipoprotein particles. They serve as solubilizers of plasma lipids, platform for enzymatic reactions and ligands for cellular receptors. ApoM is mainly associated with HDL. We have generated genetically modified mouse models that either overexpress apoM or lack the apoM gene (apoM-knock out mice) and use these models to unravel the biology of apoM. Our studies have revealed that apoM has a protective role in atherosclerosis. We are currently exploring the mechanisms in close collaborations with groups in Sweden, USA, and Germany.
Atherosclerosis in the underlying cause of ~90 % of cardiovascular deaths in the western world. We use cell cultures, human tissue biopsies collected at Rigshospitalet, and various mouse models to study basic mechanisms in atherosclerosis.
Chronic kidney disease and accelerated atherosclerosis
Chronic kidney disease leads to accumulation of waster products in plasma (uremia). During recent years it has become clear that patients with chronic kidney disease has an enormously increased risk of dying from cardiovascular disease. We have created a mouse model with chronic uremia. The development of atherosclerosis is markedly accelerated in the uremic mouse making it a unique model for studying the pathogenesis of uremic atherosclerosis. Our results have underscored that inflammation and oxidative stress in the arterial wall play a pivotal role. Currently, we are using mice with genetically modified inflammation to further unravel basic mechanism in disease progression. The studies are combined with studies of human arterial wall biopsies and plasma.
Diabetes and obesity can decrease heart function. We are interested in exploring the role of cardiac lipid accumulation. We have used human heart biopsies, a cardiac cell line and various obese and genetically modified mouse models to disclose how the ability of the heart to secrete lipoproteins can protect against development of cardiac dysfunction. Also, we are interested in how diabetes and obesity affects the cardiac metabolism of natriuretic peptides.
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