Human LiverChip® Platforms Enable Mechanistic Interrogation of Fibrosis & Steatosis in MAFLD & MASH

• We developed 3D perfused LiverChip co‑cultures using human hepatocytes and non‑parenchymal cells to model MAFLD/MASH with physiologic multicellular interactions
• TGFβ induced strong fibrosis, inflammation, and loss of hepatocyte identity, while ALK5 inhibition reversed these effects
• Chronic lipid overload reproduced metabolic stress and MASH‑like transcriptional signatures, demonstrating the model’s utility for studying disease mechanisms and therapeutic interventions.

Speakers:

HONG WANG

Scientist IV

Boehringer Ingelheim