Genetic depletion or pharmacological degradation of EZH2 attenuates renal fibrosis via suppressing Notch signaling
These findings demonstrate that epithelial EZH2 contributes to pEMT in renal tubular cells and promotes renal fibrosis, at least in part through activation of Notch signaling. Targeting EZH2 may hold potential as a therapeutic approach for chronic kidney disease.
Authors
- Shougang Zhuang
- Xinyu Du (ORCID: https://orcid.org/0000-0002-5721-7812)
- Fengchen Shen
- Jianjun Yu (ORCID: https://orcid.org/0009-0004-3892-5786)
- Xiying Hou
- Liyuan Yao
- Na Liu (ORCID: https://orcid.org/0000-0001-5806-8209)
- Yanjin Wang (ORCID: https://orcid.org/0009-0005-1484-2537)
- Chao Yu (ORCID: https://orcid.org/0000-0002-6929-6693)
Institutions
- Rhode Island Hospital (US)
- Shanghai East Hospital (CN)
Publication Details
- Journal
- Clinical Epigenetics
- Published
- 2025-12-06
- DOI
- https://doi.org/10.1186/s13148-025-02013-9
- Citations
- 1
- Primary Topic
- Renal and related cancers
- Type
- article
- Field-Weighted Citation Impact
- 0.81