ArticleExperimental and therapeutic medicine2018
Inhibition of miR-186-5p contributes to high glucose-induced injury in AC16 cardiomyocytes.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- From Type 2 Diabetes Mellitus To Diabetic Cardiomyopathy - A Systematic Review On The Role Of MicroRNA.Current diabetes reports · 2025Pooled it
- Regulatory function of HSA-miR-186-5p on interleukin-2 expression in lumbar degenerative disc disease: a case-control study and subgroups analysis.Neurosurgical review · 2026Article
- Cardiovascular Dysfunction in Type 2 Diabetes: The Role of MicroRNAs.Handbook of experimental pharmacology · 2026Review
- Emerging Biomarkers and Nanobiosensing Strategies in Diabetes.Biosensors · 2025Review
- Interaction networks among miRNA, protein, and metabolite fingerprints identify the regulatory networks and key players in the pathogenesis of diabetic cardiomyopathy.Frontiers in cell and developmental biology · 2025Article
- Relationship of lncRNA FTX and miR-186-5p levels with diabetic peripheral neuropathy in type 2 diabetes and its bioinformatics analysis.Irish journal of medical science · 2024Article
- LncRNA ANRIL Promotes Glucose Metabolism and Proliferation of Colon Cancer in a High-Glucose Environment and is Associated with Worse Outcome in Diabetic Colon Cancer Patients.Asian Pacific journal of cancer prevention : APJCP · 2024Article
- MicroRNA-186-5p inhibits H9c2 cells apoptosis induced by oxygen-glucose deprivation by targeting ERK1/2.Journal of thoracic disease · 2023Article
- Hsa_circ_0008360 sponges miR-186-5p to target CCND2 to modulate high glucose-induced vascular endothelial dysfunction.Cell cycle (Georgetown, Tex.) · 2021Article
- Epigenetics, microRNA and Metabolic Syndrome: A Comprehensive Review.International journal of molecular sciences · 2021Review
- MicroRNA‑186‑5p downregulation inhibits osteoarthritis development by targeting MAPK1.Molecular medicine reports · 2021Article
- Review
- Upregulation of miRNA-23a-3p rescues high glucose-induced cell apoptosis and proliferation inhibition in cardiomyocytes.In vitro cellular & developmental biology. Animal · 2020Article
- Diagnostic value of miR-186-5p for carotid artery stenosis and its predictive significance for future cerebral ischemic event.Diagnostic pathology · 2020Article
- Profiling and functional analysis of differentially expressed circular RNAs in high glucose-induced human umbilical vein endothelial cells.FEBS open bio · 2019Article
- MicroRNA‑186‑5p is expressed highly in ethanol‑induced cardiomyocytes and regulates apoptosis via the target gene XIAP.Molecular medicine reports · 2019Article
- Association of Serum miR-186-5p With the Prognosis of Acute Coronary Syndrome Patients After Percutaneous Coronary Intervention.Frontiers in physiology · 2019Article
- The epigenetic mechanisms of nanotopography-guided osteogenic differentiation of mesenchymal stem cells via high-throughput transcriptome sequencing.International journal of nanomedicine · 2018Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A growing body of evidence has demonstrated that microRNAs (miRs) have pivotal roles in the pathophysiological development mechanisms of diabetic cardiomyopathy (DCM). Previous studies have demonstrated that miR-186-5p was significantly decreased in DCM. In addition, it has recently been reported that an imbalance of miR-186 is associated with a variety of physiological and pathological processes. Therefore, the present study was designed to investigate the role of miR-186-5p in high glucose (HG)-induced cytotoxicity and apoptosis in AC16 cardiomyocytes. Reverse transcription-polymerase chain reaction was used to demonstrate the significant decrease in the level of miR-186-5p in HG-treated AC16 cells (P<0.05). Subsequently, it was clarified that pre-transfection with miR-186-5p mimic significantly ameliorated the effects of high glucose, which induced a significant decrease in the viability of AC16 cells (P<0.05) and increases in apoptosis, as evidenced by the appearance of apoptotic nucleus and the significant upregulation of apoptosis rate in AC16 cells (P<0.05). In addition, the significantly increased expression of caspase-3 induced by HG (P<0.01) was also reversed by miR-186-5p mimic (P<0.01). Conversely, transfection with miR-186-5p inhibitor significantly reduced the viability of AC16 cells (P<0.05) and promoted apoptosis (P<0.05) as well as the expression of caspase-3 in AC16 cells (P<0.01), indicating the beneficial role of miR-186-5p in the physiological process of HG-induced damage. In conclusion, these results suggest that the distribution of miR-186-5p contributes to HG-induced cytotoxicity and apoptosis in AC16 cardiomyocytes.
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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 Socratic graph.