ReviewThe Journal of physiology2015
Roles and post-translational regulation of cardiac class IIa histone deacetylase isoforms.
Review in The Journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Histone Deacetylase 7 protects against pathologic cardiac hypertrophy.Journal of molecular and cellular cardiology · 2026Article
- Gut Microbiota and Bacterial Extracellular Vesicles: Emerging Roles in Myocardial Remodelling and Cardiac Health.Journal of extracellular biology · 2025Review
- LMK235 ameliorates inflammation and fibrosis after myocardial infarction by inhibiting LSD1-related pathway.Scientific reports · 2024Article
- Roles of histone acetylation sites in cardiac hypertrophy and heart failure.Frontiers in cardiovascular medicine · 2023Review
- Metabolic remodeling in cardiac hypertrophy and heart failure with reduced ejection fraction occurs independent of transcription factor EB in mice.Frontiers in cardiovascular medicine · 2023Article
- Molecular perspectives in hypertrophic heart disease: An epigenetic approach from chromatin modification.Frontiers in cell and developmental biology · 2022Review
- Mechanism of histone deacetylases in cardiac hypertrophy and its therapeutic inhibitors.Frontiers in cardiovascular medicine · 2022Review
- Changes in Stress-Mediated Markers in a Human Cardiomyocyte Cell Line under Hyperglycemia.International journal of molecular sciences · 2021Article
- Casein Kinase-2 Interacting Protein-1 Regulates Physiological Cardiac HypertrophyFrontiers in physiology · 2021Article
- Nucleoporins in cardiovascular disease.Journal of molecular and cellular cardiology · 2020Review
- HDAC inhibitors and cardioprotection: Homing in on a mechanism of action.EBioMedicine · 2019Article
- Novel Insight Into the Epigenetic and Post-transcriptional Control of Cardiac Gene Expression by Thyroid Hormone.Frontiers in endocrinology · 2019Review
- Inflammation leads through PGE/EPEMBO molecular medicine · 2018Article
- Bidirectional regulation of HDAC5 by mAKAPβ signalosomes in cardiac myocytes.Journal of molecular and cellular cardiology · 2018Article
- A proteolytic fragment of histone deacetylase 4 protects the heart from failure by regulating the hexosamine biosynthetic pathway.Nature medicine · 2018Article
- β-Adrenergic Stimulation Induces Histone Deacetylase 5 (HDAC5) Nuclear Accumulation in Cardiomyocytes by B55α-PP2A-Mediated Dephosphorylation.Journal of the American Heart Association · 2017Article
- How cardiomyocytes sense pathophysiological stresses for cardiac remodeling.Cellular and molecular life sciences : CMLS · 2017Review
- Serine/Threonine Kinase 40 (Stk40) Functions as a Novel Regulator of Skeletal Muscle Differentiation.The Journal of biological chemistry · 2017Article
- A class of their own: exploring the nondeacetylase roles of class IIa HDACs in cardiovascular disease.American journal of physiology. Heart and circulatory physiology · 2016Review
- Promiscuous actions of small molecule inhibitors of the protein kinase D-class IIa HDAC axis in striated muscle.FEBS letters · 2015Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiomyocyte hypertrophy is an integral component of pathological cardiac remodelling in response to mechanical and chemical stresses in settings such as chronic hypertension or myocardial infarction. For hypertrophy to ensue, the pertinent mechanical and chemical signals need to be transmitted from membrane sensors (such as receptors for neurohormonal mediators) to the cardiomyocyte nucleus, leading to altered transcription of the genes that regulate cell growth. In recent years, nuclear histone deacetylases (HDACs) have attracted considerable attention as signal-responsive, distal regulators of the transcriptional reprogramming that in turn precipitates cardiomyocyte hypertrophy, with particular focus on the role of members of the class IIa family, such as HDAC4 and HDAC5. These histone deacetylase isoforms appear to repress cardiomyocyte hypertrophy through mechanisms that involve protein interactions in the cardiomyocyte nucleus, particularly with pro-hypertrophic transcription factors, rather than via histone deacetylation. In contrast, evidence indicates that class I HDACs promote cardiomyocyte hypertrophy through mechanisms that are dependent on their enzymatic activity and thus sensitive to pharmacological HDAC inhibitors. Although considerable progress has been made in understanding the roles of post-translational modifications (PTMs) such as phosphorylation, oxidation and proteolytic cleavage in regulating class IIa HDAC localisation and function, more work is required to explore the contributions of other PTMs, such as ubiquitination and sumoylation, as well as potential cross-regulatory interactions between distinct PTMs and between class IIa and class I HDAC isoforms.
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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.