ArticleThe Journal of clinical investigation2011
Loss of H3K4 methylation destabilizes gene expression patterns and physiological functions in adult murine cardiomyocytes.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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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
72 citing papers in PubMed, 125 citations in OpenAlex.
- Roles of different methylation modifications in cardiovascular disease.Frontiers of medicine · 2025Review
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- Integrated bioinformatics analysis reveals Netrin-1 as a key molecular link between Parkinson's disease and heart failure.Frontiers in aging neuroscience · 2025Article
- Isoprenaline Inhibits Histone Demethylase LSD1 to Induce Cardiac Hypertrophy.Cardiovascular toxicology · 2025Article
- Morphogenesis-coupled DNA repair - in mammalian embryogenesis, morphogenesis and DNA double strand break (DSB) repair are carried out simultaneously to ensure normal development.Journal of radiation research · 2024Article
- Hallmarks of cardiovascular ageing.Nature reviews. Cardiology · 2023Review
- ASH2L regulates postnatal neurogenesis through Onecut2-mediated inhibition of TGF-β signaling pathway.Cell death and differentiation · 2023Article
- Epigenetic Modification Factors and microRNAs Network Associated with Differentiation of Embryonic Stem Cells and Induced Pluripotent Stem Cells toward Cardiomyocytes: A Review.Life (Basel, Switzerland) · 2023Review
- M3 Receptor Pathway Stimulates Rapid Transcription of the CB1 Receptor Activation through Calcium Signalling and the CNR1 Gene Promoter.International journal of molecular sciences · 2023Article
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- Systems analysis of de novo mutations in congenital heart diseases identified a protein network in the hypoplastic left heart syndrome.Cell systems · 2022Article
- Fibroblast growth factor 20 attenuates pathological cardiac hypertrophy by activating the SIRT1 signaling pathway.Cell death & disease · 2022Article
- Indoxyl sulfate reduces Ito,f by activating ROS/MAPK and NF-κB signaling pathways.JCI insight · 2022Article
- Posttranslational Modifications: Emerging Prospects for Cardiac Regeneration Therapy.Journal of cardiovascular translational research · 2022Review
- Identification of Novel Genetic Variants and Comorbidities Associated With ICD-10-Based Diagnosis of Hypertrophic Cardiomyopathy Using the UK Biobank Cohort.Frontiers in genetics · 2022Article
- The Genetics and Epigenetics of Ventricular Arrhythmias in Patients Without Structural Heart Disease.Frontiers in cardiovascular medicine · 2022Review
- The roles and mechanisms of epigenetic regulation in pathological myocardial remodeling.Frontiers in cardiovascular medicine · 2022Review
- Review
- Epigenetic Regulation of Cardiomyocyte Differentiation from Embryonic and Induced Pluripotent Stem Cells.International journal of molecular sciences · 2021Review
- YTHDF2 alleviates cardiac hypertrophy via regulating Myh7 mRNA decoy.Cell & bioscience · 2021Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Histone H3 lysine 4 (H3K4me) methyltransferases and their cofactors are essential for embryonic development and the establishment of gene expression patterns in a cell-specific and heritable manner. However, the importance of such epigenetic marks in maintaining gene expression in adults and in initiating human disease is unclear. Here, we addressed this question using a mouse model in which we could inducibly ablate PAX interacting (with transcription-activation domain) protein 1 (PTIP), a key component of the H3K4me complex, in cardiac cells. Reducing H3K4me3 marks in differentiated cardiomyocytes was sufficient to alter gene expression profiles. One gene regulated by H3K4me3 was Kv channel-interacting protein 2 (Kcnip2), which regulates a cardiac repolarization current that is downregulated in heart failure and functions in arrhythmogenesis. This regulation led to a decreased sodium current and action potential upstroke velocity and significantly prolonged action potential duration (APD). The prolonged APD augmented intracellular calcium and in vivo systolic heart function. Treatment with isoproterenol and caffeine in this mouse model resulted in the generation of premature ventricular beats, a harbinger of lethal ventricular arrhythmias. These results suggest that the maintenance of H3K4me3 marks is necessary for the stability of a transcriptional program in differentiated cells and point to an essential function for H3K4me3 epigenetic marks in cellular homeostasis.
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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.