Dr. rer. medic. Hacer Sahin
Cand. med. Alexander Flasshove
Cand. med. Aaron Rodenhausen
Cand. med. Jonathan Frederik Brozat
Liver fibrosis represents a main pathophysiological outcome of nearly all chronic liver diseases, which are tightly linked to immune cell recruitment and hepatic stellate cell activation. Ultimately, progressive chronic liver diseases can result in liver cirrhosis and hepatocellular carcinoma (HCC), accounting for a large increase of morbidity and mortality worldwide.
In the wake of enormous scientific process regarding molecular interactions between parenchymal hepatic resident cells, endothelial barrier components and infiltrating leukocytes, increasing interest develops around cell- cell- interactions such as through tight junctions.
Upon injury-dependent activation of quiescent hepatic stellate cells into extracellular-matrix-producing myofibroblasts a complex inflammatory process involving extracellular remodelation and fibrotic scarring is initiated. Early and continuous leukocyte infiltration following a chemical gradient-tightly regulated by cytokines, especially chemokines- leads to local and specific extravasation, setting the constraints necessary for this inflammation.
Our group focuses on further investigation and analyzation of leukocyte transmigration and diapedesis, platelet interaction, chemotactic active soluble components and the role of tight junction proteins in the complex micro-environment of chronic liver injuries and HCC.
The group is currently funded by:
- Deutsche Krebshilfe
- Deutsche Forschungsgemeinschaft DFG
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