ArticleMolecular medicine reports2017
Overexpressed microRNA-506 and microRNA-124 alleviate H2O2-induced human cardiomyocyte dysfunction by targeting krüppel-like factor 4/5.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- MicroRNA Signatures and Machine Learning Models for Predicting Cardiotoxicity in HER2-Positive Breast Cancer Patients.Pharmaceuticals (Basel, Switzerland) · 2025Article
- High-resolution single-cell transcriptomic survey of cardiomyocytes from patients with hypertrophic cardiomyopathy.Cell proliferation · 2024Article
- Krüppel-like factor (KLF)5: An emerging foe of cardiovascular health.Journal of molecular and cellular cardiology · 2022Review
- Research Progress on the Inflammatory Effects of Long Non-coding RNA in Traumatic Brain Injury.Frontiers in molecular neuroscience · 2022Review
- Current knowledge of Krüppel-like factor 5 and vascular remodeling: providing insights for therapeutic strategies.Journal of molecular cell biology · 2021Review
- Polyphyllin Ⅲ-Induced Ferroptosis in MDA-MB-231 Triple-Negative Breast Cancer Cells can Be Protected Against by KLF4-Mediated Upregulation of xCT.Frontiers in pharmacology · 2021Article
- Circ_0030235 knockdown protects H9c2 cells against OGD/R-induced injury via regulation of miR-526b.PeerJ · 2021Article
- Overexpression of miR-124 Protects Against Neurological Dysfunction Induced by Neonatal Hypoxic-Ischemic Brain Injury.Cellular and molecular neurobiology · 2020Article
- Effects of Oxidative Stress on Protein Translation: Implications for Cardiovascular Diseases.International journal of molecular sciences · 2020Review
- Silencing of KCNQ1OT1 Decreases Oxidative Stress and Pyroptosis of Renal Tubular Epithelial Cells.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
- MicroRNA-506 Is Involved in Regulation of the Occurrence of Lipopolysaccharides (LPS)-Induced Pulpitis by Sirtuin 1 (SIRT1).Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Hyperhomocysteinemia induces vascular calcification by activating the transcription factor RUNX2 via Krüppel-like factor 4 up-regulation in mice.The Journal of biological chemistry · 2019Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Krüppel-like factors (KLFs) regulate a wide variety of cellular functions and modulate pathological processes. In the present study, a post‑translational mechanism of microRNAs (miRs) was investigated in H2O2-induced human cardiomyocyte (HCM) injury. In H2O2‑cultured HCM cells, reactive oxygen species and apoptotic cells were measured via flow cytometry. miR‑506/‑124 mimics and inhibitors were transfected to induce gain or loss of miR‑506/‑124 function. Cell proliferation was analyzed by an MTT assay. The targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay. The mRNA and protein expression levels were measured by reverse transcription‑polymerse chain reaction analysis and western blotting, respectively. The results indicated that H2O2 induced significant apoptosis and increased the concentration of reactive oxygen species (ROS) in HCMs. H2O2 markedly upregulated the expression levels of KLF4 and KLF5, and downregulated the expression levels of miR‑506 and miR‑124 in the HCMs. In addition, bioinformatics analysis showed the potential miR‑506 and miR‑124 binding sites within the 3'‑untranslated region of KLF4 and KLF5 in the HCMs. The overexpression of miR‑506 and miR‑124 inhibited the H2O2‑induced upregulation of KLF4 and KLF5 in the HCMs. The overexpression of miR‑506 and miR‑214 reversed the H2O2‑induced apoptosis and increase of ROS in the HCMs. In conclusion, the overexpression of miR‑506 and miR‑214 were confirmed to have a protective effect against H2O2‑induced HCM injury by suppressing the expression of KLF4 and KLF5.
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