ArticleESC heart failure2022
Circ_0001206 regulates miR-665/CRKL axis to alleviate hypoxia/reoxygenation-induced cardiomyocyte injury in myocardial infarction.
Article in ESC heart failure, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- The emerging roles of small nucleolar RNAs, piwi-interacting RNAs, tRNA-derived small RNAs, and circular RNAs in the regulation of cardiac hypertrophy, ischemic heart disease, and heart failure.Genes & diseases · 2026Review
- Application Advances of Lentiviral Vectors: From Gene Therapy to Vaccine Development.Molecular biotechnology · 2026Review
- CircRNA Networks in CAD: Multi-Cellular Mechanisms and Clinical Potential.International journal of general medicine · 2025Review
- Review
- Identification of circular RNAs regulating cardiomyocyte proliferation in neonatal pig hearts.JCI insight · 2024Article
- Integrin beta 3-overexpressing mesenchymal stromal cells display enhanced homing and can reduce atherosclerotic plaque.World journal of stem cells · 2023Article
- Circular RNAs: Biogenesis, Biological Functions, and Roles in Myocardial Infarction.International journal of molecular sciences · 2023Review
- Circular RNAs in organ injury: recent development.Journal of translational medicine · 2022Review
- Circ_0001206 regulates miR-665/CRKL axis to alleviate hypoxia/reoxygenation-induced cardiomyocyte injury in myocardial infarction.ESC heart failure · 2022Article
- The circRNA-miRNA/RBP regulatory network in myocardial infarction.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsMyocardial infarction (MI) is a type of cardiovascular disease caused by myocardial necrosis. Growing evidences have suggested that circular RNAs (circRNAs) play crucial roles in cardiac hypoxia/reoxygenation (H/R)-induced injury of MI. METHODS AND
resultsHypoxia/reoxygenation model of H9C2 cells was established and circ_0001206 expression was detected via quantitative real-time polymerase chain reaction. Ribonuclease R (RNase R) and Actinomycin D (Act D) assays verified the stability. Cell counting kit-8 (CCK-8), western blot, TUNEL, and flow cytometry assays evaluated cell viability and cell apoptosis. RNA pull-down, RNA binding protein immunoprecipitation (RIP), and luciferase reporter assays explored the mechanisms underlying MI. All experimental data were presented with mean ± standard deviation (SD) and P < 0.05 indicated statistical significance. Circ_0001206 was low-expressed in H9C2 cells under H/R treatment. Circ_0001206 was formed by cyclization of CRK like proto-oncogene, adaptor protein (CRKL). Circ_0001206 overexpression promoted cell viability and inhibited cardiomyocyte apoptosis. It was confirmed that circ_0001206 regulated CRKL expression via acting as a competing endogenous RNA (ceRNA) of microRNA-665 (miR-665). CRKL played a protective role in MI.
conclusionsCirc_0001206 regulates miR-665/CRKL axis to alleviate H/R-induced cardiomyocyte injury in MI. Our findings suggest that circ_0001206 might be a potential target for MI treatment.
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