ArticleOncotarget2017
The long non-coding RNA H19 promotes cardiomyocyte apoptosis in dilated cardiomyopathy.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 65 citations in OpenAlex.
- Cardiomyocyte programmed cell death in dilated cardiomyopathy: molecular crosstalk and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- The silent dialogue between cells: regulatory roles of non-coding RNAs in cardiovascular disease.Frontiers in cell and developmental biology · 2026Review
- Overview of exosomal non-coding RNAs in cardiovascular disease using high throughput sequencing.European journal of pharmacology · 2025Review
- Cardiomyopathies: The Role of Non-Coding RNAs.Non-coding RNA · 2024Review
- miRNA-133 and lncRNA-H19 expressions and their relation to serum levels of PKM2 and TGF-β in patients with systemic sclerosis.Non-coding RNA research · 2024Article
- The role and medical prospects of long non-coding RNAs in cardiovascular disease.Heart failure reviews · 2023Review
- The Role of MicroRNAs in Dilated Cardiomyopathy: New Insights for an Old Entity.International journal of molecular sciences · 2022Review
- Heart Failure Strategically Focused Research Network: Summary of Results and Future Directions.Journal of the American Heart Association · 2022Article
- Circular RNAs: New Players in Cardiomyopathy.Genes · 2022Review
- The multifaceted actions of the lncRNA H19 in cardiovascular biology and diseases.Clinical science (London, England : 1979) · 2022Review
- Long Noncoding RNAs Involved in Cardiomyocyte Apoptosis Triggered by Different Stressors.Journal of cardiovascular translational research · 2022Review
- Long non-coding RNAs and microRNAs as crucial regulators in cardio-oncology.Cell & bioscience · 2022Review
- I-κB kinase-ε deficiency improves doxorubicin-induced dilated cardiomyopathy by inhibiting the NF-κB pathway.Frontiers in physiology · 2022Article
- A genetic variant alters the secondary structure of the lncRNA H19 and is associated with dilated cardiomyopathy.RNA biology · 2021Article
- Non-coding RNAs in cardiac regeneration: Mechanism of action and therapeutic potential.Seminars in cell & developmental biology · 2021Review
- Cardiomyocyte mitochondrial dynamic-related lncRNA 1 (CMDL-1) may serve as a potential therapeutic target in doxorubicin cardiotoxicity.Molecular therapy. Nucleic acids · 2021Article
- The Emerging Role of Epigenetics in Therapeutic Targeting of Cardiomyopathies.International journal of molecular sciences · 2021Review
- The function of LncRNA-H19 in cardiac hypertrophy.Cell & bioscience · 2021Review
- Review
- Differential expression profiles of long noncoding RNAs and mRNAs in human bone marrow mesenchymal stem cells after exposure to a high dosage of dexamethasone.Stem cell research & therapy · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the previous study, we generated a rat model of dilated cardiomyopathy (DCM) induced by adriamycin and found that the expression of lncRNA H19 was significantly upregulated in myocardial tissue. The present study was aimed to investigate the potential role of H19 in the pathogenesis of adriamycin-induced DCM. H19 knockdown in the myocardium of DCM rats attenuated cardiomyocyte apoptosis and improved left ventricular structure and function. Adriamycin treatment was associated with elevated H19 and miR-675 expression and increased apoptosis in neonatal cardiomyocytes. Enforced expression of miR-675 was found to induce apoptosis in cardiomyocytes with adriamycin treatment and H19-siRNA transfection. The 3'-untranslated region of PA2G4 was cloned downstream of a luciferase reporter construct and cotransfected into HEK293 cells with miR-675 mimic. The results of luciferase assay showed that PA2G4 was a direct target of miR-675. The expression of PA2G4 was reduced in cardiomyocytes transfected with miR-675 mimic. Moreover, H19 knockdown was found to increase PA2G4 expression and suppress apoptosis in cardiomyocytes exposed to adriamycin. In conclusion, our study suggests that H19/miR-675 axis is involved in the promotion of cardiomyocyte apoptosis by targeting PA2G4, which may provide a new therapeutic strategy for the treatment of adriamycin-induced DCM.
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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.