Kif23 Promotes Myocardial Fibrosis by Suppressing Ces1d-Dependent Lipid Metabolism
Our study identifies Kif23 as a novel regulator of post-MI cardiac fibrosis. Mechanistically, Kif23 drives fibroblast proliferation through RhoA activation and exacerbates fibrogenesis by suppressing Ces1d-dependent fatty acid β-oxidation via the RhoA/ROCK1 axis. This metabolic disruption triggers pathological lipid accumulation and myofibroblast transdifferentiation. These findings nominate Kif23 as a promising therapeutic target for antifibrotic interventions.
Authors
- Honghong Chen (ORCID: https://orcid.org/0000-0001-9682-5709)
- Jialin Zhao (ORCID: https://orcid.org/0000-0002-1165-8911)
- Jun Chang (ORCID: https://orcid.org/0000-0001-6481-7130)
- Wen Zhong (ORCID: https://orcid.org/0000-0001-7623-5082)
- Caiyun Wang (ORCID: https://orcid.org/0000-0003-2542-7425)
- Xinhua Liu (ORCID: https://orcid.org/0000-0002-9972-8215)
- Yuyu Zhang (ORCID: https://orcid.org/0000-0003-3095-3083)
- Jie Xu (ORCID: https://orcid.org/0000-0001-9163-3898)
- Yajie Hu (ORCID: https://orcid.org/0000-0001-5976-3094)
- Chunxiang Fan
- Qiuyuan Huang (ORCID: https://orcid.org/0000-0003-1421-9698)
Institutions
- Shanghai University of Traditional Chinese Medicine (CN)
Publication Details
- Journal
- Hypertension
- Published
- 2025-10-13
- DOI
- https://doi.org/10.1161/hypertensionaha.125.25744
- Citations
- 1
- Primary Topic
- Cardiomyopathy and Myosin Studies
- Type
- article
- Field-Weighted Citation Impact
- 1.39