CVB3-induced P62 cleavage promotes ferroptosis through the NRF2/GPX4 axis and facilitates viral replication
This study identifies a novel mechanism whereby CVB3 exploits the cleavage of P62 to inactivate the KEAP1/NRF2/GPX4 axis, thereby driving ferroptosis and disease progression. These findings highlight the therapeutic potential of restoring P62 function and supplementing selenium to alleviate CVB3-induced pathogenesis.
Authors
- Dingding Cao (ORCID: https://orcid.org/0000-0001-9413-9430)
- Xuelai Liu
- Xiaoyu Yi
- Hailan Yao
- Feng He (ORCID: https://orcid.org/0000-0001-5692-5561)
- Zhuo Liu (ORCID: https://orcid.org/0000-0001-9343-2969)
- Sen Li (ORCID: https://orcid.org/0000-0001-7747-4253)
- Feng Miao (ORCID: https://orcid.org/0000-0002-2863-3489)
- Zhewei Liu (ORCID: https://orcid.org/0000-0002-8276-6063)
- Yiting Jiang (ORCID: https://orcid.org/0009-0001-0434-5204)
Institutions
- Capital Institute of Pediatrics (CN)
Publication Details
- Journal
- Frontiers in Microbiology
- Published
- 2025-11-21
- DOI
- https://doi.org/10.3389/fmicb.2025.1675667
- Primary Topic
- Ferroptosis and cancer prognosis
- Type
- article
- Field-Weighted Citation Impact
- 0.00