Targeting STE20-type kinase MST3 improves metabolic dysfunction-associated steatohepatitis without affecting hepatocellular carcinoma development in mice
Our findings in the selected mouse model of MASH-HCC suggest that MST3 is dispensable for hepatocarcinogenesis, yet its antagonism dampens diet-induced metabolic dysfunction and effectively attenuates MASH severity, challenging the prevailing assumption that targeting MASH driver genes alone is sufficient to prevent HCC development in the context of obesity.
Institutions
- Oslo University Hospital (NO)
- Shanghai Jiao Tong University (CN)
- Ionis Pharmaceuticals (United States) (US)
- Renji Hospital (CN)
- Sahlgrenska University Hospital (SE)
- University Medical Center Freiburg (DE)
- Institute of Medical Microbiology and Hygiene (DE)
- University of Gothenburg (SE)
Publication Details
- Journal
- BMC Medicine
- Published
- 2026-03-24
- DOI
- https://doi.org/10.1186/s12916-026-04812-0
- Primary Topic
- Hippo pathway signaling and YAP/TAZ
- Type
- article
- Field-Weighted Citation Impact
- 0.00