Our research focuses on the molecular mechanisms controlling systemic iron metabolism and its disruption in human disease. Every year, millions of patients worldwide are affected by systemic iron overload or deficiency, and our knowledge of the underlying mechanisms and their clinical consequences is poorly understood.
An important goal of our research is to understand the regulatory circuits that maintain systemic iron homeostasis. We focus on the iron hormone hepcidin and its receptor, ferroportin. Since both excess hepcidin (leading to iron deficiency anemia) and hepcidin deficiency (causing iron overload) must be avoided, a central focus of our work is to understand the hepcidin/ferroportin regulatory axis. This is achieved through network-based analyses, as well as integration of transcriptome and proteome data, genome-wide screens, and studies in disease models.
Furthermore, we are interested in diseases in which iron deficiency or iron overload contribute to organ pathologies. An important focus here is to investigate the consequences of iron accumulation in immune cells (e.g., tumor-associated macrophages; TAMs) of the tumor microenvironment. Our research focuses on reprogramming TAMs to a proinflammatory anti-cancer phenotype by applying superoxide iron nanoparticles (SPIONs) in in vivo tumor models.
Rare anemias represent another focus of our research. These congenital blood disorders belong to a broad spectrum of very rare diseases - affecting less than 1000 people in Germany. Our patient-oriented research aims to continuously improve the diagnosis and treatment strategies of rare hematological diseases. To this end, we investigate the molecular causes of the individual diseases with the aim of identifying promising approaches for future therapies. Together with our colleagues from nationwide hospitals, we lead the registry studies for patients with rare anemias of the Society for Pediatric Oncology and Hematology.
