Fibrotic and Immunosuppressive Tumor Microenvironment

Our research investigates how the fibrotic and immunosuppressive tumor microenvironment promotes metastatic tumor growth in the liver. We focus on the dynamic interactions between cancer cells, fibroblasts, and immune cells that shape extracellular matrix remodeling and influence tumor progression. Using advanced technologies such as spatial transcriptomics, single-cell sequencing, and in vivo modeling, we aim to identify the cellular and molecular networks that drive metastasis in steatotic and fibrotic livers.

Endoplasmic Reticulum Chaperone in Liver Diseases

Our group investigates the role of endoplasmic reticulum (ER) chaperones in hepatic proteostasis and how their dysfunction contributes to chronic liver diseases. We are particularly interested in how ER stress and redox imbalance contribute to the development of ALD, liver fibrosis, and liver cancer. Through mechanistic studies using genetically modified mouse models, cellular systems, and human samples, we explore how ER-resident proteins such as ERdj5 regulate oxidative stress, fibrogenesis, and cell death pathways, providing new insights into therapeutic strategies for chronic liver diseases.

Extracellular Vesicle

Our research explores how metabolic dysfunction-associated steatotic liver disease (MASLD) affects systemic pathophysiology through extracellular vesicle-mediated inter-organ communication. We investigate the molecular cargo and functional roles of hepatocyte-derived EVs under metabolic stress, focusing on how these vesicles modulate immune responses, fibroblast activation, and tumor behavior within the liver.

Beyond the liver, we aim to elucidate hepatocyte-derived EVs influence distant organs. Integrating in vivo models, single-cell transcriptomics, and EV microRNA profiling, we seek to define EV-driven molecular pathways that connect metabolic liver dysfunction to multi-organ complications, such as diabetic kidney disease and diabetic retinopathy.