Clusterin protects against HFpEF by inhibiting UCHL1-mediated NLRP3 deubiquitylation and inflammasome activation
This study reveals a novel regulatory mechanism through which CLU alleviates HFpEF by modulating the UCHL1-NLRP3 signaling axis. The findings provide new insight into the anti-inflammatory and anti-fibrotic roles of CLU and suggest that CLU and its derived peptide hold translational potential as therapeutic candidates for HFpEF.
Authors
- Yang Sl
- Xiaoxu Kang
- Bing Hu (ORCID: https://orcid.org/0000-0001-5085-3114)
- Xixuan Wang (ORCID: https://orcid.org/0000-0003-3564-7616)
- Xinbo Wang (ORCID: https://orcid.org/0000-0003-1956-6963)
- Cheng Zhang (ORCID: https://orcid.org/0000-0003-2962-0839)
- Lang Chen (ORCID: https://orcid.org/0000-0001-7032-2513)
- Lihong Liu (ORCID: https://orcid.org/0000-0003-4817-3173)
- Jiangling Yu
- Rui Chang (ORCID: https://orcid.org/0000-0002-9820-8218)
- Lili Gong
Institutions
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- China-Japan Friendship Hospital (CN)
- Peking Union Medical College Hospital (CN)
- Beijing Friendship Hospital (CN)
Publication Details
- Journal
- Frontiers in Pharmacology
- Published
- 2026-01-13
- DOI
- https://doi.org/10.3389/fphar.2025.1704023
- Primary Topic
- Clusterin in disease pathology
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Natural Science Foundation of China