ANKRD1 aggravates renal ischaemia‒reperfusion injury via promoting TRIM25‐mediated ubiquitination of ACSL3
Ankyrin repeat domain 1 (ANKRD1) is rapidly activated in renal ischaemia‒reperfusion injury (IRI) models in vivo and in vitro. ANKRD1 knockdown mitigates kidney damage and preserves renal function. Ferroptosis contributes to the deteriorating function of ANKRD1 in renal IRI. ANKRD1 promotes acyl-coenzyme A synthetase long-chain family member 3 (ACSL3) degradation via the ubiquitin‒proteasome pathway. The E3 ligase tripartite motif containing 25 (TRIM25) is responsible for ANKRD1-mediated ubiquitination of ACSL3.
Authors
- Haochong Hu
- Tao Qiu (ORCID: https://orcid.org/0000-0002-1410-7795)
- Jiangqiao Zhou (ORCID: https://orcid.org/0000-0002-6118-0020)
- Chenyang Kong
- Shangting Han (ORCID: https://orcid.org/0000-0002-1429-4009)
- Cheng Fan (ORCID: https://orcid.org/0000-0002-3471-6221)
- Qi Chen (ORCID: https://orcid.org/0000-0002-3022-5310)
- Jun Li (ORCID: https://orcid.org/0000-0001-8243-5267)
- Jiayu Guo (ORCID: https://orcid.org/0009-0008-7015-6437)
- Fangyou Lin (ORCID: https://orcid.org/0000-0001-7369-7855)
- Jiefu Zhu
- Yiting Liu (ORCID: https://orcid.org/0009-0006-0620-3847)
- Tianyu Wang
Institutions
- Southwest Medical University (CN)
- Wuhan University (CN)
- Renmin Hospital of Wuhan University (CN)
Publication Details
- Journal
- Clinical and Translational Medicine
- Published
- 2024-09-01
- DOI
- https://doi.org/10.1002/ctm2.70024
- Citations
- 11
- Primary Topic
- Ferroptosis and cancer prognosis
- Type
- article
- Field-Weighted Citation Impact
- 4.61
Funders
- National Natural Science Foundation of China