Myeloid-specific S100A8/A9 deficiency attenuates atrial fibrillation through prevention of TLR4/NF-kB-mediated immune cell recruitment and inflammation
Myeloid-derived S100A8/A9 amplifies AF by promoting monocyte recruitment and inflammation via the TLR4/NF-κB axis. Targeting this pathway may offer a promising therapeutic strategy for AF prevention and treatment.
Authors
- Jing Wang (ORCID: https://orcid.org/0000-0003-1140-6690)
- Hua Shen (ORCID: https://orcid.org/0000-0001-9060-8172)
- Qing Wang (ORCID: https://orcid.org/0009-0003-7328-8762)
- Yufeng Zhang (ORCID: https://orcid.org/0000-0002-3154-7979)
- Guifang Wang (ORCID: https://orcid.org/0000-0002-2203-0222)
Institutions
- Shanghai Chest Hospital (CN)
- Chinese PLA General Hospital (CN)
- Shanghai University of Traditional Chinese Medicine (CN)
- Shanghai Changzheng Hospital (CN)
- Shuguang Hospital (CN)
- Xinxiang Central Hospital (CN)
Publication Details
- Journal
- Frontiers in Immunology
- Published
- 2025-09-04
- DOI
- https://doi.org/10.3389/fimmu.2025.1623486
- Primary Topic
- S100 Proteins and Annexins
- Type
- article
- Field-Weighted Citation Impact
- 0.00