Jung-Chin Chang

CardioShift resolves cell-to-cell functional heterogeneity in hiPSC-derived cardiomyocytes by accounting for nested variance, revealing hidden subpopulations and condition-dependent phenotypes.

The paper develops an in vitro MASH model to study metabolite crosstalk between Kupffer cells and hepatocytes, identifying itaconate as a key mediator of liver disease progression.

This study shows that hepatic stellate cells enhance HCC proliferation through HIF-dependent metabolic changes and H2O2 signaling.

This study develops a method to generate and expand hepatobiliary organoids from adult human hepatocytes, which retain liver function and can model liver diseases.