ArticleMolecular biology of the cell2008
YY1 protects cardiac myocytes from pathologic hypertrophy by interacting with HDAC5.
Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 69 citations in OpenAlex.
- A novel Notch and WNT signaling mechanism contribute to paediatric DCM: a pathway to new therapeutics.bioRxiv : the preprint server for biology · 2025Article
- Pim3 up-regulation by YY1 contributes to diabetes-induced cardiac hypertrophy and heart failure.Iranian journal of basic medical sciences · 2025Article
- Postprandial cardiac hypertrophy is sustained by mechanics, epigenetic, and metabolic reprogramming in pythons.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- HDAC5 inhibition attenuates ventricular remodeling and cardiac dysfunction.Orphanet journal of rare diseases · 2023Article
- Review
- Trajectory reconstruction identifies dysregulation of perinatal maturation programs in pluripotent stem cell-derived cardiomyocytes.Cell reports · 2023Article
- Myocardial brain-derived neurotrophic factor regulates cardiac bioenergetics through the transcription factor Yin Yang 1.Cardiovascular research · 2023Article
- The Protective Role of Yin-Yang 1 in Cardiac Injury and Remodeling After Myocardial Infarction.Journal of the American Heart Association · 2021Article
- Histone deacetylases in modulating cardiac disease and their clinical translational and therapeutic implications.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Systemic Bioinformatic Analyses of Nuclear-Encoded Mitochondrial Genes in Hypertrophic Cardiomyopathy.Frontiers in genetics · 2021Article
- Lysine acetylation of cytoskeletal proteins: Emergence of an actin code.The Journal of cell biology · 2020Review
- Network integration and modelling of dynamic drug responses at multi-omics levels.Communications biology · 2020Article
- YY1 control of mitochondrial-related genes does not account for regulation of immunoglobulin class switch recombination in mice.European journal of immunology · 2020Article
- Understanding Failure and Improving Treatment Using HDAC Inhibitors for Prostate Cancer.Biomedicines · 2020Review
- Contribution of Increased Expression of Yin Yang 2 to Development of Cardiomyopathy.Frontiers in molecular biosciences · 2020Article
- The Two Sides of YY1 in Cancer: A Friend and a Foe.Frontiers in oncology · 2019Review
- The effect of melatonin on cardio fibrosis in juvenile rats with pressure overload and deregulation of HDACs.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018Article
- YY1 Expression Is Sufficient for the Maintenance of Cardiac Progenitor Cell State.Stem cells (Dayton, Ohio) · 2017Article
- Exosomes from pediatric dilated cardiomyopathy patients modulate a pathological response in cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
YY1 is a transcription factor that can repress or activate the transcription of a variety of genes. Here, we show that the function of YY1 as a repressor in cardiac myocytes is tightly dependent on its ability to interact with histone deacetylase 5 (HDAC5). YY1 interacts with HDAC5, and overexpression of YY1 prevents HDAC5 nuclear export in response to hypertrophic stimuli and the increase in cell size and re-expression of fetal genes that accompany pathological cardiac hypertrophy. Knockdown of YY1 results in up-regulation of all genes present during fetal development and increases the cell size of neonatal cardiac myocytes. Moreover, overexpression of a YY1 deletion construct that does not interact with HDAC5 results in transcription activation, suggesting that HDAC5 is necessary for YY1 function as a transcription repressor. In support of this relationship, we show that knockdown of HDAC5 results in transcription activation by YY1. Finally, we show that YY1 interaction with HDAC5 is dependent on the HDAC5 phosphorylation domain and that overexpression of YY1 reduces HDAC5 phosphorylation in response to hypertrophic stimuli. Our results strongly suggest that YY1 functions as an antihypertrophic factor by preventing HDAC5 nuclear export and that up-regulation of YY1 in human heart failure may be a protective mechanism against pathological hypertrophy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.