Research

The major interest of our research is the identification of therapeutic targets for metabolic dysfunction-associated steatohepatitis (MASH) and metabolic dysfunction-associated alcohol-related liver disease (MetALD)-associated liver fibrosis. My research interest focuses on following topics.

1. MASH: Validation of therapeutic targets for metabolic dysfunction-associated liver fibrosis

2. Hepatic Stellate Cells (HSCs): Phenotypic changes of HSCs in MASLD progression

3.  Human Liver Organoids: Generation of 3D human liver spheroids to study liver fibrosis induced by metabolic stress

Human liver spheroids to study 

MASH "in a dish"

Currently, there is no effective treatment for obesity and alcohol associated liver diseases, partially due to the lack of translational human models. 

We established a protocol to generate 3D human liver spheroids that contain all major liver cell types and mimic “livers in a dish.” Using this system, we induce metabolic- and alcohol-associated hepatic steatosis, inflammation, and fibrosis. 

Liver myofibroblasts

Development of liver fibrosis is caused by fibrogenic myofibroblasts that are not present in the normal liver, but rather activate from liver resident mesenchymal cells in response to chronic toxic or cholestatic injury.  Hepatic stellate cell (HSC) and portal fibroblasts were identified as primary sources of hepatic myofibroblasts in fibrotic liver.  We investigate potential phenotypes of hepatic stellate cells and portal fibroblasts activated in response to toxic and cholestatic liver injury and outlined the possible mechanisms of their activation, and pathways of their targeting for antifibrotic therapy.