ANKRD1 aggravates renal ischaemia‒reperfusion injury via promoting TRIM25-mediated ubiquitination of ACSL3
Shangting Han , Jiayu Guo , Chenyang Kong , Jun Li , Fangyou Lin , Jiefu Zhu , Tianyu Wang , Qi Chen , Yiting Liu , Haochong Hu , Tao Qiu , Fan Cheng , Jiangqiao Zhou
Clinical and Translational Medicine ›› 2024, Vol. 14 ›› Issue (9) : e70024
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. |
ACSL3 / ANKRD1 / ferroptosis / renal ischaemic‒reperfusion injury / TRIM25 / ubiquitination
2024 The Author(s). Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics.
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