HMC ameliorates myocardial ischaemia–reperfusion injury through suppressing cuproptosis via the de‐ubiquitination and stabilization of ATP7A
Our work unveils a ubiquitin-regulated copper homeostasis axis in MI/RI. By targeting MARCHF7-ATP7A interaction, HMC sustains copper export machinery to combat cuproptosis-driven injury. These findings position HMC as a novel therapeutic candidate for MI/RI through regulating ubiquitination-dependent regulation of copper homeostasis.
Authors
- Min Wei (ORCID: https://orcid.org/0000-0003-4005-1331)
- Bin Chen (ORCID: https://orcid.org/0000-0001-9851-3928)
- Chuanlong Zhu (ORCID: https://orcid.org/0000-0002-0657-828X)
- Mai Liu
- Jiru Zhang (ORCID: https://orcid.org/0000-0001-6322-8764)
- Hai‐Jian Sun (ORCID: https://orcid.org/0000-0002-7791-5335)
- Guo Chen (ORCID: https://orcid.org/0000-0001-8886-1873)
- Jia‐Bao Su
- You‐Yi Zhuang
- Yunfeng Ji (ORCID: https://orcid.org/0000-0002-9676-8211)
- Le Yang
- Xue‐Xue Zhu (ORCID: https://orcid.org/0009-0003-9847-6882)
Institutions
- Jiangnan University (CN)
- China Pharmaceutical University (CN)
- Wuxi Fourth People's Hospital (CN)
Publication Details
- Journal
- British Journal of Pharmacology
- Published
- 2025-08-14
- DOI
- https://doi.org/10.1111/bph.70171
- Citations
- 1
- Primary Topic
- Cardiac Ischemia and Reperfusion
- Type
- article
- Field-Weighted Citation Impact
- 1.47
Funders
- National Natural Science Foundation of China
- Jiangnan University
- Natural Science Foundation of Jiangsu Province
- Wuxi Municipal Bureau on Science and Technology
- Fundamental Research Funds for the Central Universities