Cardiomyocyte USP20 alleviates septic cardiomyopathy by deubiquitinating and inhibiting NLRP3 activity
Cardiomyocyte-derived USP20 is crucial in septic cardiomyopathy progression. NLRP3 is identified as a substrate protein of USP20. USP20 deubiquitinates NLRP3 by removing K63-linked ubiquitin at K243 residue via its active site C154, disrupting the interaction between NLRP3 and ASC, suppressing NLRP3 activation and subsequent pyroptosis. USP20 may serve as a novel therapeutic target for managing septic cardiomyopathy.
Authors
- Weijian Huang (ORCID: https://orcid.org/0000-0003-2958-134X)
- Zu‐Yao Yang (ORCID: https://orcid.org/0000-0003-2386-2431)
- Kai Ye (ORCID: https://orcid.org/0000-0002-2851-6741)
- Lingfeng Zhong (ORCID: https://orcid.org/0009-0002-3938-8826)
- Yunxuan Chen (ORCID: https://orcid.org/0009-0007-3791-9933)
- Yucong Zhang (ORCID: https://orcid.org/0000-0002-2991-5066)
- Shanshan Dai (ORCID: https://orcid.org/0000-0001-5124-5882)
- Ziyi Huang (ORCID: https://orcid.org/0000-0002-1678-3463)
- Rongqin Zheng (ORCID: https://orcid.org/0000-0002-7129-8436)
- Xueli Cai (ORCID: https://orcid.org/0000-0003-1670-3539)
- Xiangtao Zheng (ORCID: https://orcid.org/0009-0000-3975-1416)
Institutions
- Wenzhou Medical University (CN)
- First Affiliated Hospital of Wenzhou Medical University (CN)
Publication Details
- Journal
- Clinical and Translational Medicine
- Published
- 2025-10-01
- DOI
- https://doi.org/10.1002/ctm2.70494
- Primary Topic
- Ubiquitin and proteasome pathways
- Type
- article
- Field-Weighted Citation Impact
- 0.00