Beyond molecular chaperoning: AHA1 reprograms autophagy flux through direct ATP5A1 interaction in ischemic neuronal injury
This study reveals a novel, non-canonical function for AHA1 as a pathological driver in ischemic stroke. By directly interacting with ATP5A1, AHA1 links transcriptional stress responses to mitochondrial bioenergetic failure and excessive autophagy. Targeting the AHA1-ATP5A1 axis represents a promising therapeutic strategy to inhibit maladaptive mitophagy and protect against neurological outcomes.
Authors
- Ke Meng (ORCID: https://orcid.org/0000-0002-2460-4728)
- Xinran Ge
- Xiaowei Zhang (ORCID: https://orcid.org/0000-0002-8373-3570)
- Li Liu (ORCID: https://orcid.org/0000-0001-7948-1975)
- Chang Liu (ORCID: https://orcid.org/0000-0002-5428-370X)
- Yujie Jia (ORCID: https://orcid.org/0000-0001-5559-3614)
- Duo Jin
Institutions
- First Affiliated Hospital of Liaoning Medical University (CN)
- Jiangjin Central Hospital (CN)
- Jinzhou Medical University (CN)
Publication Details
- Journal
- Redox Biology
- Published
- 2025-11-08
- DOI
- https://doi.org/10.1016/j.redox.2025.103920
- Citations
- 1
- Primary Topic
- Autophagy in Disease and Therapy
- Type
- article
- Field-Weighted Citation Impact
- 1.35