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ERIKSSON LABORATORY

Eriksson laboratory at the Division of Vascular Biology focuses on identifying mechanisms that regulate blood vessel formation and function. The aim is to find new ways of interfering with these processes to treat human disease. To this end, we combine developmental studies with models of human disease and apply the most recent technologies in molecular medicine.

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KAROLINSKA INSTITUTET

Karolinska Institutet is one of the world’s leading medical universities. Our vision is to advance knowledge about life and strive towards better health for all.


As a university, KI is Sweden’s single largest centre of medical academic research and offers the country’s widest range of medical courses and programmes.

Since 1901 the Nobel Assembly at Karolinska Institutet has selected the Nobel laureates in Physiology or Medicine.

RESEARCH HIGHLIGHT

Recent publications from Eriksson lab

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May, 2017

Here, we demonstrate in experimental mouse models of DKD that renal VEGF-B expression correlates with the severity of disease. Inhibiting VEGF-B signaling in DKD mouse models reduces renal lipotoxicity, re-sensitizes podocytes to insulin signaling, inhibits the development of DKD-associated pathologies, and prevents renal dysfunction. Further, we show that elevated VEGF-B levels are found in patients with DKD, suggesting that VEGF-B antagonism represents a novel approach to treat DKD.

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September, 2012

Type 2 diabetes is a chronic disease that affects more than 310 million people worldwide, about 90% of whom display insulin resistance. This study demonstrates, in several animal models of type 2 diabetes, that genetic and pharmacological inhibition of signalling by vascular endothelial growth factor B (VEGF-B) can limit the accumulation of fats in the muscles and reverse adverse metabolic consequences of type 2 diabetes, including insulin resistance.

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April, 2010

VEGF-B, a vascular endothelial growth factor that is highly expressed in heart, skeletal muscle and brown adipose tissue, has been found to have an unexpected role in targeting lipids to peripheral tissues. Mice lacking VEGF-B accumulate lower amounts of lipids in muscle, heart and brown adipose tissue, and instead shunt them to white adipose tissue. The involvement of VEGF-B in redistributing lipids suggest possible novel strategies for modulating lipid accumulation in diabetes, obesity and cardiovascular diseases.

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Ulf Eriksson

Professor of Vascular Biology

Department of Medical Biochemistry & Biophysics

Biomedicum 6D, Solnavägen 9, 171 65, Solna

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