ArticleBioscience reports2021
Long-chain noncoding RNA-GAS5/hsa-miR-138-5p attenuates high glucose-induced cardiomyocyte damage by targeting CYP11B2.
Article in Bioscience reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- From Type 2 Diabetes Mellitus To Diabetic Cardiomyopathy - A Systematic Review On The Role Of MicroRNA.Current diabetes reports · 2025Pooled it
- Established and Emerging Roles of Epigenetic Regulation in Diabetic Cardiomyopathy.Diabetes/metabolism research and reviews · 2025Review
- LncRNA Growth Arrest Specific 5 Promotes Glucose Metabolism Reprogramming Via the IGF2BP1/SIX1 Axis and Inhibits Ferroptosis of Endothelial Progenitor Cells Via the miR-23a-3p/SLC7A11 Axis in Coronary Heart Disease.Anatolian journal of cardiology · 2025Article
- The Role of miR-138 in Cardiovascular Diseases.BioMed research international · 2025Review
- Irbesartan May Ameliorate Ventricular Remodeling by Inhibiting CREB-Mediated Cardiac Aldosterone Synthesis in Rats with Myocardial Infarction.International journal of molecular sciences · 2024Article
- The interregulatory circuit between non-coding RNA and apoptotic signaling in diabetic cardiomyopathy.Non-coding RNA research · 2024Review
- Bone marrow mesenchymal stem cells-derived exosomal lncRNA GAS5 mitigates heart failure by inhibiting UL3/Hippo pathway-mediated ferroptosis.European journal of medical research · 2024Article
- Epigenetics in diabetic cardiomyopathy.Clinical epigenetics · 2024Review
- Article
- LncRNAs in oncogenic microenvironment: from threat to therapy.Frontiers in cell and developmental biology · 2024Review
- The Role of Epicardial Adipose Tissue-Derived MicroRNAs in the Regulation of Cardiovascular Disease: A Narrative Review.Biology · 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
- The role of non-coding RNAs in myocarditis: a narrative review.Annals of translational medicine · 2022Review
- Expression Profiles of Differentially Expressed Circular RNAs and circRNA-miRNA-mRNA Regulatory Networks in SH-SY5Y Cells Infected with Coxsackievirus B5.International journal of genomics · 2022Article
- Identification of biomarkers, pathways, and potential therapeutic targets for heart failure using next-generation sequencing data and bioinformatics analysis.Therapeutic advances in cardiovascular diseaseArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveDiabetic cardiomyopathy (DCM) is one of the complications experienced by patients with diabetes. In recent years, long noncoding RNAs (lncRNAs) have been investigated because of their role in the progression of various diseases, including DCM. The purpose of the present study was to explore the role of lncRNA GAS5 in high glucose (HG)-induced cardiomyocyte injury and apoptosis. MATERIALS AND
methodsWe constructed HG-induced AC16 cardiomyocytes and a streptozotocin (STZ)-induced rat diabetes model. GAS5 was overexpressed and knocked out at the cellular level, and GAS5 was knocked down by lentiviruses at the animal level to observe its effect on myocardial injury. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of GAS5. Cell proliferation and apoptosis after GAS5 knockout were detected by CCK-8, TUNEL, and flow cytometry assays. ELISA was used to detect the changes in myocardial enzyme content in cells and animal myocardial tissues during the action of GAS5 on myocardial injury.
resultsGAS5 expression was up-regulated in HG-treated AC16 cardiomyocytes and the rat diabetic myocardial injury model. The down-regulation of GAS5 could inhibit HG-induced myocardial damage. This work proved that the down-regulation of GAS5 could reverse cardiomyocyte injury and apoptosis by targeting miR-138 to down-regulate CYP11B2.
conclusionWe confirmed for the first time that the down-regulation of GAS5 could reverse CYP11B2 via the miR-138 axis to reverse HG-induced cardiomyocyte injury. This research might provide a new direction for explaining the developmental mechanism of DCM and potential targets for the treatment of myocardial injury.
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