IL4I1 attenuates myocardial infarction by inhibiting macrophage ferroptosis via the I3P/AHR/NRF2 signaling pathway
We identify a novel cardioprotective axis wherein macrophage-derived IL4I1 catalyzes the production of I3P, activating AHR-NRF2 signaling to suppress ferroptosis, thereby mitigating post-MI inflammation, adverse remodeling, and cardiac dysfunction. Targeting IL4I1 and I3P represents a promising therapeutic strategy for ischemic heart disease.
Authors
- Yan Ding (ORCID: https://orcid.org/0000-0003-3119-9529)
- Rui Shen (ORCID: https://orcid.org/0000-0002-5704-4632)
- Kunwu Yu (ORCID: https://orcid.org/0000-0003-2414-5960)
- Chen Dong (ORCID: https://orcid.org/0000-0002-0084-9130)
- Chengliang Pan (ORCID: https://orcid.org/0000-0002-0223-7461)
- Qiutang Zeng (ORCID: https://orcid.org/0000-0002-7748-4651)
- Jiangmei Zhang
Institutions
- Wuhan Union Hospital (CN)
- Union Hospital (CN)
Publication Details
- Journal
- International Immunopharmacology
- Published
- 2025-09-03
- DOI
- https://doi.org/10.1016/j.intimp.2025.115393
- Citations
- 5
- Primary Topic
- Ferroptosis and cancer prognosis
- Type
- article
- Field-Weighted Citation Impact
- 7.59
Funders
- Innovative Research Group Project of the National Natural Science Foundation of China
- National Natural Science Foundation of China