Knockdown of suppressor of glucose by autophagy (SOGA1) alleviates the progression of non-alcoholic steatohepatitis (NASH) by reducing hepatocyte senescence through regulating AMPK/mTOR-mediated mitochondrial homeostasis
Lijing Yan, Huanhuan Sun, Tianyu Wang, Yuling Chen, Peijie Li · 2026
Read Knockdown of suppressor of glucose by autophagy (SOGA1) alleviates the progression of non-alcoholic steatohepatitis (NASH) by reducing hepatocyte senescence through regulating AMPK/mTOR-mediated mitochondrial homeostasis by Lijing Yan, Huanhuan Sun, Tianyu Wang, Yuling Chen, Peijie Li (2026) in the Tower of Babel, a free online library of public-domain works preserved in clean, searchable text. No sign-up. The full text is served as a plain-text file at a predictable URL, where text is present: https://antarctic-labs.com/tower-of-babel/pmc-13410608.txt.
Description
Lijing Yan and colleagues studied a liver protein in fatty liver disease in 2026. The protein helps control fat and energy use in the liver. Its role in the severe form of fatty liver disease was unclear. That severe form brings inflammation and scarring. The team fed mice a high-fat diet to model the disease. The protein rose in their liver tissue. In lab cells, the team then silenced the protein's gene. They tracked inflammation, scarring signs, cell aging, and cell powerhouses.
Silencing lowered inflammation and scarring markers. Aging markers in liver cells also fell. Signals from silenced cells calmed scar-forming cells in a dish. The pathway work pointed to better upkeep of cell powerhouses. Aging liver cells release signals that wake scar-forming cells. In live mice, gene silencing slowed disease progress. The authors name the protein as a possible drug target.
Catalog record
| CREATOR | Lijing Yan, Huanhuan Sun, Tianyu Wang, Yuling Chen, Peijie Li |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 60 KB |
| VERSION | 1.0 |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |