UQCRC1 downregulation impairs cognitive function in mice <i>via</i> AMPK inactivation
This study identifies AMPK as a pivotal metabolic orchestrator of mitochondrial-lysosomal functional crosstalk and reveals its non-canonical function in maintaining neuronal homeostasis <i>via</i> coordinated regulation of autophagic flux and redox balance. Our findings propose AMPK-driven interorganelle communication as a modifiable therapeutic target for addressing cognitive decline resulting from mitochondrial dysfunction.
Authors
- Jing Zhang (ORCID: https://orcid.org/0000-0003-3234-9293)
- Hong Li (ORCID: https://orcid.org/0000-0002-9192-1213)
- Zhuoyan Wu (ORCID: https://orcid.org/0000-0002-3304-9180)
- Fuhai Bai
- Zonghong Long
- Feng Ceng
Institutions
- Army Medical University (CN)
- Affiliated Hospital of North Sichuan Medical College (CN)
- Xinqiao Hospital (CN)
Publication Details
- Journal
- PeerJ
- Published
- 2025-08-15
- DOI
- https://doi.org/10.7717/peerj.19873
- Primary Topic
- Autophagy in Disease and Therapy
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Natural Science Foundation of China