My research focuses on β-cell/islet biology and type 1 diabetes. I have a passion for translational diabetes research aiming at identifying molecular targets with future therapeutic potential and biomarkers for disease prediction and progression. My principal research interests lie in the field of cellular and molecular biology of the insulin-producing β-cells but extends into other areas, such as functional genomics, inflammatory biomarkers, and non-coding RNA. My key areas of expertise are in vitro and ex vivo models of β-cell dysfunction and death. The long-term perspective is to preserve β-cell function in individuals with type 1 diabetes.
Cathepsin proteases in type 1 diabet
on understanding the functions of the lysosomal cathepsin proteases in the β cells and their implication in type 1 diabetes.
Functional genomics in type 1 diabetes
Investigation of candidate genes for their functional role(s) in the β cell. We want to translate observations from genome-wide association studies (GWAS) into understanding type 1 diabetes pathogenesis at the β-cell level.
Non-coding RNAs in type 1 diabetes
Focus on understanding the role of non-coding RNAs in β cells and diabetes. We have already identified microRNAs and long non-coding RNAs expressed and regulated in pancreatic islets and β-cell lines.
Inflammatory biomarkers in diabetes
Investigation of circulating pro- and anti-inflammatory markers to identify biomarkers of development, progression and treatment of type 1 diabetes.
1. Project title: Involvement of Cathepsin S in type 1 diabetes development and progression
Aim: To investigate if cathepsin S affects β-cell function and type 1 diabetes development. Using cellular and mouse models of type 1 diabetes we will examine whether inhibition of cathepsin S affects β-cell function and protects against diabetes development. We will also examine if the circulating level of cathepsin S can predict disease development and progression.
Collaborators: Karsten Buschard, Jesper Johannesen, Decio L Eizirik.
Aim: To characterize the cathepsin proteases and to understand their implication in β-cell dysfunction and type 1 diabetes development. Our approach is to combine functional gene knock-down/overexpression experiments in β-cell lines with information from gene-knockout mice and clinical studies.
Collaborators: Decio L Eizirik, Aashiq H Mirza, Thomas Reinheckel.