Basic Mechanisms of MASH Progression
Nov
2026
Description
This session explores emerging mechanisms that govern the development and progression of metabolic dysfunction–associated steatotic liver disease and steatohepatitis. Presentations will examine how hepatocyte metabolic programs, macrophage efferocytosis, bile acid signaling, natural killer cell dysfunction, aging-related ferroptosis, and fibrosis-associated cellular states contribute to liver injury and fibrogenesis. The session will also highlight translational insights from preclinical models, including the potential of FGF21-based therapy to promote fibrosis regression and prevent hepatocellular carcinoma.
Presentations
8:00 AM
- 8:15 AM
Convention Center - Bluebird Ballroom 1B
Aging-Impaired RXRα Acetylation Drives GCH1 Loss and Ferroptosis-Promoted Senescence in MASH
Mayank Choubey, Associate Scientist | Abstract Presenter
8:15 AM
- 8:30 AM
Convention Center - Bluebird Ballroom 1B
CD74+ efferocytic macrophages suppress cathepsin C expression through methionine metabolic reprogramming in MASLD and liver fibrosis
Yang Xiao, PhD | Abstract Presenter
8:30 AM
- 8:45 AM
Convention Center - Bluebird Ballroom 1B
Long-acting FGF21 analogue pegozafermin induces fibrosis reversal and prevents hepatocellular carcinoma in a murine MASH cirrhosis model
Zaur Abilov, MD | Abstract Presenter
8:45 AM
- 9:00 AM
Convention Center - Bluebird Ballroom 1B
High Salt Supplementation of a MASH-inducing Diet Causes Lean MASH Phenotype with Increased Hepatic Urea Cycle Activity and EIF5A Hypusination
Shaopeiwen Luo, Ph.D. | Abstract Presenter
9:00 AM
- 9:15 AM
Convention Center - Bluebird Ballroom 1B
Multi-omic and functional characterization of fibrosis-associated hepatocyte programs in MASLD
JeongSu Park, PhD | Abstract Presenter
9:15 AM
- 9:30 AM
Convention Center - Bluebird Ballroom 1B
Primary Cilia–Hedgehog Signaling Regulates Hepatocyte Plasticity
Raquel Maeso-Diaz, PhD | Abstract Presenter
