ArticleMolecular medicine (Cambridge, Mass.)2017
The Histone Methyltransferase Mixed Lineage Leukemia (MLL) 3 May Play a Potential Role on Clinical Dilated Cardiomyopathy.
Article in Molecular medicine (Cambridge, Mass.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Methylation-centric epigenetic regulation in dilated cardiomyopathy: mechanisms, metabolic interplay, and translational potential.Frontiers in cardiovascular medicine · 2026Review
- In Vivo Models of Cardiovascular Disease:Biomedicines · 2025Review
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Ferroptosis in Cancer: Epigenetic Control and Therapeutic Opportunities.Biomolecules · 2024Review
- Distinct Roles for COMPASS Core Subunits Set1, Trx, and Trr in the Epigenetic Regulation ofInternational journal of molecular sciences · 2023Article
- The functions of SET domain bifurcated histone lysine methyltransferase 1 (SETDB1) in biological process and disease.Epigenetics & chromatin · 2023Review
- The Roles of Histone Lysine Methyltransferases in Heart Development and Disease.Journal of cardiovascular development and disease · 2023Review
- Histone acetyltransferase P300 deficiency promotes ferroptosis of vascular smooth muscle cells by activating the HIF-1α/HMOX1 axis.Molecular medicine (Cambridge, Mass.) · 2023Article
- The epigenetic regulatory mechanisms of ferroptosis and its implications for biological processes and diseases.MedComm · 2023Review
- Integration of epigenetic regulatory mechanisms in heart failure.Basic research in cardiology · 2023Review
- Effects of DNA, RNA, and Protein Methylation on the Regulation of Ferroptosis.International journal of biological sciences · 2023Review
- Lpt, trr, and Hcf regulate histone mono- and dimethylation that are essential for Drosophila heart development.Developmental biology · 2022Article
- The histone demthylase KDM3A protects the myocardium from ischemia/reperfusion injury via promotion of ETS1 expression.Communications biology · 2022Article
- Dilated cardiomyopathy: a new insight into the rare but common cause of heart failure.Heart failure reviews · 2022Review
- Targeting Ferroptosis as a Novel Approach to Alleviate Aortic Dissection.International journal of biological sciences · 2022Article
- 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
- Exploring Key Genes to Construct a Diagnosis Model of Dilated Cardiomyopathy.Frontiers in cardiovascular medicine · 2022Article
- Review
- Downregulation of Filamin a Expression in the Aorta Is Correlated With Aortic Dissection.Frontiers in cardiovascular medicine · 2021Article
- Upregulation of IRF9 Contributes to Pulmonary Artery Smooth Muscle Cell Proliferation During Pulmonary Arterial Hypertension.Frontiers in pharmacology · 2021Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone modifications play a critical role in the pathological processes of dilated cardiomyopathy (DCM). While the role and expression pattern of histone methyltransferases (HMTs), especially mixed lineage leukemia (MLL) families on DCM are unclear. To this end, twelve normal and fifteen DCM heart samples were included in the present study. A murine cardiac remodelling model was induced by transverse aortic constriction (TAC). Real-time PCR was performed to detect the expression levels of MLL families in the mouse and human left ventricles. The mRNA level of MLL3 was significantly increased in the mouse hearts treated by TAC surgery. Compared with normal hearts, higher mRNA and protein level of MLL3 was detected in the DCM hearts, and its expression level was closely associated with left ventricular end systolic diameter (LVEDD) and left ventricular ejection fraction (LVEF). However, the expression level of other MLL families (MLL, MLL2, MLL4, MLL5, SETD1A, and SETD1B) had no obvious change between control and DCM hearts or remodeled mouse hearts. Furthermore, the di-methylated histone H3 lysine 4 (H3K4me2) but not H3K4me3 was significantly increased in the DCM hearts. The protein levels of Smad3, GATA4, EGR1, which might regulate by MLL3, were remarkably elevated in the DCM hearts. Our hitherto unrecognized findings indicate that MLL3 has a potential role on pathological processes of DCM via regulating H3K4me2 and the expression of Smad3, GATA4, and EGR1.
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