Heart failure & cardiomyopathies
INO80-Dependent Remodeling of Transcriptional Regulatory Network Underlies the Progression of Heart Failure
An erratum to this article was published (Circulation, 2 Apr 2024 ↗)
Authors' conclusion
In summary, our findings shed light on the INO80-dependent remodeling of the chromatin landscape and transcriptional networks as a major mechanism underlying cardiac dysfunction in heart failure
Study context
- Population
- Human heart samples and genetic mouse models of HF
- Outcome
- Role of INO80 in cardiac function and HF (expression, overexpression and deletion effects)
Main finding
As reported in the abstract
- INO80 abundantly expressed in mature cardiomyocytes; expression further increased in mouse and human HF
- Cardiomyocyte-specific Ino80 overexpression induced HF within 4 days
- INO80 overexpression reshaped nucleosomal landscape, remodeling core transcription factors, notably MEF2 family, whose target genes associated with cardiac function
- Conditional cardiomyocyte-specific Ino80 deletion in established mouse HF model: remarkable preservation of cardiac function
Original publication
INO80-Dependent Remodeling of Transcriptional Regulatory Network Underlies the Progression of Heart Failure. Circulation. Published 28 December 2023. doi:10.
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