ArticleBioscience reports2019
Long non-coding RNA MEG3 serves as a ceRNA for microRNA-145 to induce apoptosis of AC16 cardiomyocytes under high glucose condition.
Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- From Type 2 Diabetes Mellitus To Diabetic Cardiomyopathy - A Systematic Review On The Role Of MicroRNA.Current diabetes reports · 2025Pooled it
- Programmed cell death protein 4 (PDCD4): a pleiotropic regulator in cardiovascular diseases.Journal of physiology and biochemistry · 2026Review
- The interregulatory circuit between non-coding RNA and apoptotic signaling in diabetic cardiomyopathy.Non-coding RNA research · 2024Review
- The study of the mechanism of non-coding RNA regulation of programmed cell death in diabetic cardiomyopathy.Molecular and cellular biochemistry · 2024Review
- Epigenetics in diabetic cardiomyopathy.Clinical epigenetics · 2024Review
- LncRNA and mRNA expression characteristic and bioinformatic analysis in myocardium of diabetic cardiomyopathy mice.BMC genomics · 2024Article
- LncRNA HCG18 affects diabetic cardiomyopathy and its association with miR-9-5p/IGF2R axis.Heliyon · 2024Article
- Construction of a potentially functional long noncoding RNA-microRNA-mRNA network in diabetic cardiomyopathy.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2024Article
- LncRNA MEG3: Targeting the Molecular Mechanisms and Pathogenic causes of Metabolic Diseases.Current medicinal chemistry · 2024Review
- Inhibition of MEG3 ameliorates cardiomyocyte apoptosis and autophagy by regulating the expression of miRNA-129-5p in a mouse model of heart failure.Redox report : communications in free radical research · 2023Article
- Biological functions of CRTC2 and its role in metabolism-related diseases.Journal of cell communication and signaling · 2023Review
- Dysregulation of Inflammation, Oxidative Stress, and Glucose Metabolism-Related Genes and miRNAs in Visceral Adipose Tissue of Women with Type 2 Diabetes Mellitus.Medical science monitor : international medical journal of experimental and clinical research · 2023Article
- Cardiovascular complications of diabetes: role of non-coding RNAs in the crosstalk between immune and cardiovascular systems.Cardiovascular diabetology · 2023Review
- Effects of non-coding RNAs and RNA-binding proteins on mitochondrial dysfunction in diabetic cardiomyopathy.Frontiers in cardiovascular medicine · 2023Review
- The multifaceted biology of lncR-Meg3 in cardio-cerebrovascular diseases.Frontiers in genetics · 2023Review
- Unveiling the Vital Role of Long Non-Coding RNAs in Cardiac Oxidative Stress, Cell Death, and Fibrosis in Diabetic Cardiomyopathy.Antioxidants (Basel, Switzerland) · 2022Review
- Review
- Regulation of Oxidative Stress by Long Non-Coding RNAs in Vascular Complications of Diabetes.Life (Basel, Switzerland) · 2022Review
- CircularRNA circ_0071269 knockdown protects against from diabetic cardiomyopathy injury by microRNA-145/gasdermin A axis.Bioengineered · 2022Article
- lncRNA MEG3 modulates hepatic stellate cell activation by sponging miR‑145 to regulate PPARγ.Molecular medicine reports · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic cardiomyopathy (DCM) is one of the most serious complications of diabetes, but its pathogenesis remains largely unclear. In the present study, we aimed to explore the potential role of long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) and to investigate the underlying mechanisms in human AC16 cardiomyocytes under high glucose (HG) condition. The results demonstrated that MEG3 was overexpressed in HG-treated AC16 cells, and MEG3 knockdown suppressed the HG-induced apoptosis in AC16 cells. Mechanistically, MEG3 directly binds to miR-145 in AC16 cells, thereby up-regulating the expression of PDCD4. Rescue experiments showed that the role of MEG3 in HG-treated AC16 cells was partly dependent on its suppression on miR-145. In summary, our findings suggested that the role of MEG3 in HG-treated human cardiomyocytes is to serve as a competing endogenous RNA (ceRNA), which negatively regulates miR-145. These findings may provide a valuable and promising therapeutic target for the treatment of DCM in the future.
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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.