TAB2 deficiency induces dilated cardiomyopathy by promoting mitochondrial calcium overload in human iPSC-derived cardiomyocytes
In summary, TAB2 abatement cardiomyocytes mimic dilated cardiomyopathy in vitro. This finding emphasizes the importance of using a human model to study the underlying mechanisms of this specific disease. More importantly, the discovery of a unique pathogenic pathway introduces a new notion for the future management of dilated cardiomyopathy.
Authors
- Mengduan Liu
- Wanrong Fu (ORCID: https://orcid.org/0000-0002-7521-5204)
- Wenrui Sun
- Jianzeng Dong (ORCID: https://orcid.org/0000-0001-7299-7805)
- Yangyang Liu (ORCID: https://orcid.org/0000-0001-8296-7095)
- Shuang Li (ORCID: https://orcid.org/0000-0002-3970-1061)
- Xiaoyan Zhao (ORCID: https://orcid.org/0000-0003-2468-6767)
- Jianchao Zhang (ORCID: https://orcid.org/0000-0002-3269-4639)
- Xiaowei Li (ORCID: https://orcid.org/0009-0005-9996-1999)
Institutions
- Zhengzhou University (CN)
- Beijing Anzhen Hospital (CN)
- First Affiliated Hospital of Zhengzhou University (CN)
- Henan Agricultural University (CN)
Publication Details
- Journal
- Molecular Medicine
- Published
- 2025-02-04
- DOI
- https://doi.org/10.1186/s10020-025-01103-x
- Citations
- 2
- Primary Topic
- Cardiac Fibrosis and Remodeling
- Type
- article
- Field-Weighted Citation Impact
- 2.78
Funders
- National Natural Science Foundation of China
- China Postdoctoral Science Foundation