Deletion of MAPL ameliorates septic cardiomyopathy by mitigating mitochondrial dysfunction
Our results reveal that MAPL promotes cardiac injury/dysfunction and inflammation in SCM. Deficiency or knockdown of MAPL alleviates SCM by reducing drp1 SUMOylation as well as drp1-mediated mitochondrial dysfunction. These findings suggest that targeting MAPL may represent a therapeutic strategy for patients with SCM.
Authors
- Zhaohua Cai (ORCID: https://orcid.org/0000-0001-8642-9040)
- Fei Zhuang (ORCID: https://orcid.org/0000-0002-2332-6543)
- Linghong Shen (ORCID: https://orcid.org/0000-0002-4387-4109)
- Qingqi Ji
- Huanhuan Huo (ORCID: https://orcid.org/0000-0002-3040-2882)
- Xia Wang (ORCID: https://orcid.org/0000-0002-7750-1167)
- Ben He (ORCID: https://orcid.org/0000-0001-5567-4115)
- Xiying Huang
- Yinghua Wang
- Yi Li (ORCID: https://orcid.org/0000-0001-7995-9385)
- Yi Jiang (ORCID: https://orcid.org/0000-0001-9600-5065)
Institutions
- Shanghai Jiao Tong University (CN)
- Shanghai Chest Hospital (CN)
Publication Details
- Journal
- Journal of Translational Medicine
- Published
- 2024-11-11
- DOI
- https://doi.org/10.1186/s12967-024-05836-x
- Citations
- 7
- Primary Topic
- Mitochondrial Function and Pathology
- Type
- article
- Field-Weighted Citation Impact
- 1.64
Funders
- National Natural Science Foundation of China