CXCL1 Promotes Fibrotic Remodeling in Atrial Fibrillation via Activation of TXNDC5 and Endoplasmic Reticulum Stress
CXCL1 promotes atrial fibrosis through the activation of ERS and upregulation of TXNDC5, potentially contributing to atrial remodeling and the pathogenesis of AF. Targeting the CXCL1-ERS-TXNDC5 axis may offer a novel therapeutic approach for preventing and treating AF-related atrial fibrosis.
Authors
- Jungang Nie (ORCID: https://orcid.org/0009-0002-1718-5438)
- Wen Yuan (ORCID: https://orcid.org/0000-0001-9586-1601)
- Kun Huang (ORCID: https://orcid.org/0000-0003-1641-1472)
- Chenglong Wu (ORCID: https://orcid.org/0000-0001-6008-999X)
- Siyang Yu (ORCID: https://orcid.org/0000-0002-4007-0383)
- Ru Ying (ORCID: https://orcid.org/0000-0001-6443-3903)
- Ran Yin
Institutions
- Nanchang University (CN)
- First Affiliated Hospital of Nanchang University (CN)
Publication Details
- Journal
- Cardiovascular Therapeutics
- Published
- 2025-01-01
- DOI
- https://doi.org/10.1155/cdr/7892499
- Primary Topic
- Atrial Fibrillation Management and Outcomes
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Natural Science Foundation of China
- Natural Science Foundation of Jiangxi Province
- Nanchang University