Cellular Catalysts of Fibrosis: Stromal Signals, Exosomes, and Inflammation in the Diseased Liver

Description

This session highlights emerging mechanisms by which non-parenchymal cells (NPCs), particularly hepatic stellate cells (HSCs), orchestrate liver fibrogenesis in the context of metabolic dysfunction and chronic injury. Presentations will examine the impact of exosomal microRNAs, inflammasome activation, mitochondrial stress, and Notch/YAP signaling on HSC activation and fibrotic progression. Together, these studies illuminate how cell–cell communication, immune-metabolic crosstalk, and novel therapeutic targets shape liver fibrosis and hepatocellular carcinoma risk.

Journey Maps

Presentations

5:15 PM - 5:30 PM
May 18 2026
Washington, D.C.

Hepatic stellate cell Notch contributes to liver fibrosis in metabolic dysfunction-associated steatohepatitis

Vik Meadows, PhD , Abstract Presenter
Basic Science
5:30 PM - 5:45 PM
May 18 2026
Washington, D.C.

Development of a YAP PROTAC with anti-fibrotic potential

Yasuko Iwakiri, PhD, FAASLD , Abstract Presenter
Basic Science

Objectives

  • Explain the roles of hepatic stellate cells, exosomes, and inflammatory signaling in promoting liver fibrosis and modulating regeneration.
  • Discuss how mitochondrial dysfunction and metabolic stress contribute to HSC activation and fibrogenesis.
  • Evaluate emerging anti-fibrotic strategies, including exosome-based therapies and targeted degradation of fibrogenic transcriptional regulators.