ECHS1-NOX4 interaction suppresses rotenone-induced dopaminergic neurotoxicity through inhibition of mitochondrial ROS production
ECHS1 counteracted dopaminergic neurodegeneration through inhibition of mtROS and restoration of mitochondrial function via interaction with NOX4. Given the central role of mitochondrial dysfunction in PD pathogenesis, elucidating the role of ECHS1 holds great promise for uncovering novel therapeutic targets.
Authors
- Nobutaka Hattori (ORCID: https://orcid.org/0000-0002-2034-2556)
- Liyan Hou (ORCID: https://orcid.org/0000-0002-4350-8176)
- Haitao Ge
- Hong Su (ORCID: https://orcid.org/0000-0002-4673-6449)
- Taku Hatano (ORCID: https://orcid.org/0000-0002-6808-0444)
- Zirui Zhao
- Ruonan Wang (ORCID: https://orcid.org/0000-0002-7574-1810)
- Qingshan Wang (ORCID: https://orcid.org/0000-0003-4115-552X)
- Jie Zhao (ORCID: https://orcid.org/0000-0001-5687-9286)
Institutions
- Dalian Medical University (CN)
- RIKEN Center for Brain Science (JP)
- Juntendo University (JP)
Publication Details
- Journal
- Free Radical Biology and Medicine
- Published
- 2025-03-01
- DOI
- https://doi.org/10.1016/j.freeradbiomed.2025.02.048
- Citations
- 7
- Primary Topic
- Mitochondrial Function and Pathology
- Type
- article
- Field-Weighted Citation Impact
- 5.64