Nature Communications (Jul 2022)
Targeting transcription in heart failure via CDK7/12/13 inhibition
- Austin Hsu,
- Qiming Duan,
- Daniel S. Day,
- Xin Luo,
- Sarah McMahon,
- Yu Huang,
- Zachary B. Feldman,
- Zhen Jiang,
- Tinghu Zhang,
- Yanke Liang,
- Michael Alexanian,
- Arun Padmanabhan,
- Jonathan D. Brown,
- Charles Y. Lin,
- Nathanael S. Gray,
- Richard A. Young,
- Benoit G. Bruneau,
- Saptarsi M. Haldar
Affiliations
- Austin Hsu
- Gladstone Institutes
- Qiming Duan
- Gladstone Institutes
- Daniel S. Day
- Whitehead Institute for Biomedical Research
- Xin Luo
- Amgen Research
- Sarah McMahon
- Gladstone Institutes
- Yu Huang
- Gladstone Institutes
- Zachary B. Feldman
- Vanderbilt University Medical Center
- Zhen Jiang
- Gladstone Institutes
- Tinghu Zhang
- Department of Cancer Biology, Dana-Farber Cancer Institute
- Yanke Liang
- Department of Biological Chemistry & Molecular Pharmacology, Harvard Medical School
- Michael Alexanian
- Gladstone Institutes
- Arun Padmanabhan
- Gladstone Institutes
- Jonathan D. Brown
- Vanderbilt University Medical Center
- Charles Y. Lin
- Baylor College of Medicine
- Nathanael S. Gray
- Department of Cancer Biology, Dana-Farber Cancer Institute
- Richard A. Young
- Whitehead Institute for Biomedical Research
- Benoit G. Bruneau
- Gladstone Institutes
- Saptarsi M. Haldar
- Gladstone Institutes
- DOI
- https://doi.org/10.1038/s41467-022-31541-8
- Journal volume & issue
-
Vol. 13,
no. 1
pp. 1 – 11
Abstract
In this study, Hsu et al. show that inhibition of CDK7/12/13 attenuates maladaptive transcriptional activation in cultured cardiomyocytes and a mouse model of heart failure, suggesting that targeting the transcription machinery might be a therapeutic approach to treat heart failure with reduced ejection fraction.
