ArticleJournal of cellular and molecular medicine2019
Long non-coding RNA MEG3 knockdown attenuates endoplasmic reticulum stress-mediated apoptosis by targeting p53 following myocardial infarction.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- SGPP2 Ameliorates Chronic Heart Failure by Attenuating ERS via the SIRT1/AMPK Pathway.Current issues in molecular biology · 2026Article
- Long non-coding RNAs as molecular hubs integrating inflammatory and osteogenic pathways in calcific aortic valve disease.Frontiers in cardiovascular medicine · 2026Review
- Walras modulates sex-dependent endoplasmic reticulum stress in cardiomyopathy.Frontiers in physiology · 2026Article
- LncRNA MEG3 exacerbates diabetic cardiomyopathy via activating pyroptosis signaling pathway.Frontiers in pharmacology · 2025Article
- MIR193BHG inhibits the proliferation, migration and invasion of trophoblasts by upregulating p53.Experimental and therapeutic medicine · 2024Article
- Long non-coding RNA-mediated modulation of endoplasmic reticulum stress under pathological conditions.Journal of cellular and molecular medicine · 2024Review
- Control of endothelial cell function and arteriogenesis by MEG3:EZH2 epigenetic regulation of integrin expression.Molecular therapy. Nucleic acids · 2024Article
- Fructose induced KHK-C can increase ER stress independent of its effect on lipogenesis to drive liver disease in diet-induced and genetic models of NAFLD.Metabolism: clinical and experimental · 2023Article
- LncRNAs and CircRNAs in Endoplasmic Reticulum Stress: A Promising Target for Cardiovascular Disease?International journal of molecular sciences · 2023Review
- Non-coding RNA mediates endoplasmic reticulum stress-induced apoptosis in heart disease.Heliyon · 2023Review
- Fructose Induced KHK-C Increases ER Stress and Modulates Hepatic Transcriptome to Drive Liver Disease in Diet-Induced and Genetic Models of NAFLD.bioRxiv : the preprint server for biology · 2023Article
- The multifaceted biology of lncR-Meg3 in cardio-cerebrovascular diseases.Frontiers in genetics · 2023Review
- Evaluating the Role of lncRNAs in the Incidence of Cardiovascular Diseases in Androgenetic Alopecia Patients.Cardiovascular toxicology · 2022Review
- Long Noncoding RNAs Involved in Cardiomyocyte Apoptosis Triggered by Different Stressors.Journal of cardiovascular translational research · 2022Review
- The Networks of Noncoding RNAs and Their Direct Molecular Targets in Myocardial Infarction.International journal of biological sciences · 2022Review
- Transcription Factors Involved in the Development and Prognosis of Cardiac Remodeling.Frontiers in pharmacology · 2022Review
- Silencing lncRNA 93358 Inhibits the Apoptosis of Myocardial Cells in Myocardial Infarction Rats by Inducing the Expression of SLC8A1.BioMed research international · 2022Article
- LncRNA MEG3: Potential stock for precision treatment of cardiovascular diseases.Frontiers in pharmacology · 2022Review
- High fiber diet attenuate the inflammation and adverse remodeling of myocardial infarctionFrontiers in microbiology · 2022Article
- Maternally expressed 3 inhibits the biological activity of oral squamous cell carcinoma SCC25 and CAL27 cell lines.Oncology letters · 2021Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mounting evidence has indicated that long non-coding RNA maternally expressed gene 3 (lncRNA MEG3) regulates cell apoptosis, and is involved in a variety of diseases. However, its exact role in myocardial infarction (MI) has not been fully elucidated. In the present study, we firstly observed that the expression levels of the lncRNA MEG3 in infarct hearts and hypoxic neonatal mice ventricular myocytes (NMVMs) were up-regulated by quantitative real-time PCR (qRT-PCR). Then, we knocked down lncRNA MEG3 by lentiviral delivery in the myocardial border region following multipoint injection. Following 28 days of MI, the lncRNA MEG3 knockdown mice indicated better cardiac function, and less cardiac remodelling by ultrasonic cardiogram and histological analysis. In addition, we indicated that lncRNA MEG3 knockdown reduced myocyte apoptosis and reactive oxygen species production in MI mice model and hypoxic NMVMs. Furthermore, we revealed that knockdown of lncRNA MEG3 protected against endoplasmic reticulum stress (ERS)-mediated myocardial apoptosis including the induction of PERK-eIF2α and caspase 12 pathways. At last, we provided evidence that p53 was identified as a protein target of lncRNA MEG3 to regulate NF-κB- and ERS-associated apoptosis. Taken collectively, our findings demonstrated that lncRNA MEG3 knockdown exerted cardioprotection by reducing ERS-mediated apoptosis through targeting p53 post-MI.
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