Expertise:

Cell culture techniques

Proteomics (LFQ, Activity-based)

Biochemical assays

Molecular biology techniques

Background in chemical engineering, biotechnology and molecular biology

PhD Project: Lipid hydrolysis in hepatic stellate cell activation

Metabolic dysfunction-associated fatty liver disease (MAFLD) encompasses a spectrum of liver conditions including hepatic steatosis (“fatty liver”) and metabolic dysfunction-associated steatohepatitis (MASH). The progression of MASH to advanced fibrosis, leading to cirrhosis and liver cancer poses a global health threat since hepatocellular carcinoma (HCC) is among the top five causes of cancer death worldwide.^{1, 2} Since the prevalence of MAFLD is rising and approaches one third of the global adult population³ research on its progression to severe liver conditions is crucial. 

The key event in emerging liver fibrosis is the scaring of damaged liver tissue. Scaring is driven by a specialized cell type called hepatic stellate cells (HSCs). In healthy livers, quiescent HSCs only make up a small percentage of all liver cells and function as the main storage for retinols. Unresolved liver damage facilitates a complete change of their phenotype and restructuring of their lipid storages over time. This transdifferentiation into so-called myofibroblasts is called “activation”. 

In my project (which is part of the special research program “SFB Lipid Hydrolysis”) we aim to elucidate the metabolic changes of HSCs and hepatocytes during liver disease and progression. Specifically, we are interested in the lipid metabolism of HSCs during their activation. We use (genetically modified) human liver cell lines as a model to study the lipid hydrolysis pathway, especially the roles of ATGL, CGI-58 and their interaction partners with standard biochemical assays, RT-qPCR, high-resolution mass spectrometry and further methods. 

¹Wang, Shuang, and Scott L. Friedman. "Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH)." Science translational medicine 15.716 (2023): eadi0759.

² Huang, Daniel Q., Hashem B. El-Serag, and Rohit Loomba. "Global epidemiology of NAFLD-related HCC: trends, predictions, risk factors and prevention." Nature reviews Gastroenterology & hepatology 18.4 (2021): 223-238.

³ Le, Michael H., et al. "2019 Global NAFLD prevalence: a systematic review and meta-analysis." Clinical Gastroenterology and Hepatology 20.12 (2022): 2809-2817.