Dot1L Promotes Stress-Induced Cardiac Hypertrophy in Mice via Tbx6
Dot1L-H3K79 dimethylation-Tbx6 axis facilitates pressure overload-induced cardiac hypertrophy. Targeting Dot1L may be a promising therapeutic strategy for heart failure.
Authors
- Shengkai Zuo (ORCID: https://orcid.org/0000-0003-0040-4470)
- Jiao Liu (ORCID: https://orcid.org/0000-0002-9371-0778)
- Chenghao Xuan (ORCID: https://orcid.org/0000-0002-0179-3781)
- Yuxuan Jin (ORCID: https://orcid.org/0000-0001-8997-9291)
- Dandan Huang (ORCID: https://orcid.org/0009-0002-3503-5855)
- Jiangping Song (ORCID: https://orcid.org/0000-0002-9488-7823)
- Kai Zhang (ORCID: https://orcid.org/0000-0003-2800-0531)
- Bei Wang (ORCID: https://orcid.org/0000-0001-5587-5451)
- Jinying Zhang
- Ying Yu (ORCID: https://orcid.org/0000-0002-6476-1752)
- Chengsen Mu
- Qian Liu (ORCID: https://orcid.org/0000-0002-2788-6222)
Institutions
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- First Affiliated Hospital of Zhengzhou University (CN)
- Fu Wai Hospital (CN)
- Tianjin Medical University (CN)
Publication Details
- Journal
- Circulation Research
- Published
- 2025-06-30
- DOI
- https://doi.org/10.1161/circresaha.124.324940
- Citations
- 3
- Primary Topic
- Cardiac Fibrosis and Remodeling
- Type
- article
- Field-Weighted Citation Impact
- 4.16