Kim Ravnskjær

Kim Ravnskjaer was appointed Assistant Professor at the Department of Biochemistry and Molecular Biology (BMB) in Spring 2015. He earned his PhD-degree from the University of Southern Denmark in 2006 and joined the laboratory of Prof. Marc Montminy at the Salk Institute for Biological Studies in La Jolla (US). At Salk, Kim published several papers on the hormonal regulation and dysregulation of hepatic transcription factors and their target genes in various mouse models of Type 2 diabetes.

At the Department of Biochemistry and Molecular Biology, Kim Ravnskjaer and his team focus on the development of NASH and liver fibrosis in the context of obesity and diabetes. In their studies they explore cellular and molecular mechanisms driving the development of liver fibrosis in human and mice. The aim of their work is the advancement of new methods for early detection and for treatment of the deadly disease. 

Kim Ravnskjaer is member of the Danish Diabetes Academy (DDA), the European Association for the Study of Diabetes (EASD), and is co-founder of the The Research Unit for Functional Genomics and Metabolism. He was recently awarded stipends from the European Foundation for the Study of Diabetes (EFDS), the European Commission, and the Danish Council for Independent Research.

Kim is co-founder and member of the management team of the newly established DNRF Center of Excellence 'ATLAS' (Center for Functional Genomic and Tissue Plasticity). The center is directed by Prof. Susanne Mandrup and is a cross-faculty collaboration aimed at combining functional genomics, preclinical and clinical studies of tissue plasticity in hepatic and adipose tissues in obesity and metabolic disease.

Head of research: Assistant Professor Kim Ravnskjær

Research group:
Academic staff Ann-Britt Marcher

PhD Fellow Sofie Marchsteiner Bendixen

Cellular Plasticity in the Healthy and Fibrotic liver

Non-alcoholic steatohepatitis (NASH) is the hepatic manifestation of the metabolic syndrome and has become a global epidemic. NASH is characterized by hepatic lipid accumulation and chronic inflammation. NASH is associated with massive scarring of the liver (liver fibrosis) and is a leading cause of liver cirrhosis, liver failure and liver cancer. Despite the prevalence and severity of the disease only little is known about the molecular mechanisms underlying the development of NASH and liver cirrhosis.

In our projects, we investigate how distinct hepatic cell populations communicate and undergo substantial transitions during the progression from a healthy to a cirrhotic liver.

We study the disease by taking functional genomics, histological as well as physiological approaches to analyze various animal models of obesity, diabetes and NASH. Key techniques in our laboratory include the development and use of transgenic mouse models, in vivo delivery of shRNAs by adeno-associated virus, cell type-specific transcriptomics and chromatin analysis by next-generation sequencing, single-cell transcriptomics, immunofluorescence and confocal fluorescence microscopy. Bioinformatics analysis allows us to explore large genomics and transcriptomics data sets and identify gene regulatory networks and disease mechanisms. Hereby, we create detailed molecular maps of NASH development and attain a deeper understanding of liver cell biology, disease pathogenesis and progression.

Current projects:

1. Cell type-specific analysis of gene regulatory networks and chromatin dynamics in vivo during the development and regression of experimental liver fibrosis in transgenic mice.

2. Single cell RNA sequencing (scRNAseq) analysis of hepatic cell populations and their plasticity during NASH progression.

3. Function and regulation of NASH-associated 7TM-receptors in hepatic stellate cells.

4. Cellular mechanisms underlying 'fibrotic memory'.

Selected publications

Hepatic Insulin Resistance Following Chronic Activation of the CREB Coactivator CRTC2.
Hogan MF, Ravnskjaer K, Matsumura S, Huising MO, Hull RL, Kahn SE, Montminy M. J Biol Chem. 2015 290(43), 25997-6006.

Glucagon regulates gluconeogenesis through KAT2B and WDR5 mediated epigenetic effects,
Ravnskjaer K, Hogan M, Lackey D, Tora L, Dent SY, Olefsky J, Montminy M, J Clin Invest. 2013, 123(10), 4318-4328.

Class IIa Histone Deacetylases Are Hormone-Activated Regulators of FOXO and Mammalian Glucose Homeostasis,
Mihaylova MM, Vasquez DS, Ravnskjaer K, Denechaud PD, Yu RT, Alvarez JG, Downes M, Evans RM, Montminy M, Shaw RJ. Cell. 2011, 145(4), 607-21.

A full list of publications by assistant professor Kim Ravnskjær can be found here.

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