Mammalian Ste20-like kinase 1 regulates AMPK to mitigate the progression of non-alcoholic fatty liver disease
The regulatory axis involving MST1-mediated AMPK phosphorylation emerges as a promising therapeutic modality for modulating hepatic sterol metabolism. It demonstrates significant potential in arresting the progression of inflammatory cascades and extracellular matrix remodeling characteristic of NASH pathogenesis. Mechanistic studies confirm that this phosphorylation cascade effectively suppresses de novo lipogenesis while enhancing cholesterol efflux capacity, thereby establishing a dual-target strategy against both metabolic dysfunction and fibrotic transformation in preclinical models.
Authors
- Yanru Ren (ORCID: https://orcid.org/0000-0001-6745-9471)
- Jie Ma (ORCID: https://orcid.org/0000-0002-3900-1903)
- Chenglei Zhang (ORCID: https://orcid.org/0000-0001-6494-0040)
- Jiarui Li (ORCID: https://orcid.org/0000-0002-9340-3962)
- Jianning Li (ORCID: https://orcid.org/0000-0002-9560-3896)
- Yuanyuan Wu (ORCID: https://orcid.org/0000-0002-6253-7773)
- Yi Yang (ORCID: https://orcid.org/0009-0003-5459-844X)
- Lijuan Wang (ORCID: https://orcid.org/0009-0000-3957-8860)
- Yan Li (ORCID: https://orcid.org/0000-0001-7801-0821)
Institutions
- Ningxia Medical University (CN)
- Ningxia Medical University General Hospital (CN)
Publication Details
- Journal
- European journal of medical research
- Published
- 2025-04-17
- DOI
- https://doi.org/10.1186/s40001-025-02557-9
- Citations
- 2
- Primary Topic
- Liver Disease Diagnosis and Treatment
- Type
- article
- Field-Weighted Citation Impact
- 2.71
Funders
- National Natural Science Foundation of China
- Natural Science Foundation of Ningxia Province
- Key Research and Development Program of Ningxia