FOXO1-NMNAT3 axis dysregulation promotes doxorubicin cardiotoxicity: NAD <sup>+</sup> replenishment as a redox-targeted antioxidant therapy
This study establishes the dysregulation of the FOXO1-NMNAT3 axis as a key mechanism underlying NAD<sup>+</sup> depletion in DIC. Targeting this axis through NAD<sup>+</sup> replenishment, particularly by activating NMNAT3, offers a novel redox-based therapeutic strategy against DIC.
Authors
- Fang Cheng (ORCID: https://orcid.org/0000-0002-8260-9244)
- Hongli Xiong
- Kai Yu (ORCID: https://orcid.org/0000-0002-7102-9826)
- Yemiao Chen (ORCID: https://orcid.org/0000-0001-5397-1407)
- Chong Chen (ORCID: https://orcid.org/0000-0002-6787-0495)
- Jianbo Li (ORCID: https://orcid.org/0000-0001-8965-0138)
- Ying Zhu (ORCID: https://orcid.org/0000-0003-4158-8093)
- Minzhu Zhao (ORCID: https://orcid.org/0000-0003-1798-5208)
- Qi Wang (ORCID: https://orcid.org/0000-0003-1058-5068)
Institutions
- Chongqing Technology and Business University (CN)
- Chongqing University (CN)
- Chongqing Public Health Medical Center (CN)
- Chongqing Medical University (CN)
Publication Details
- Journal
- Redox Report
- Published
- 2025-09-29
- DOI
- https://doi.org/10.1080/13510002.2025.2565033
- Citations
- 3
- Primary Topic
- FOXO transcription factor regulation
- Type
- article
- Field-Weighted Citation Impact
- 2.42