ArticleMetabolic brain disease2023
CircZfp609 contributes to cerebral infarction via sponging miR-145a-5p to regulate BACH1.
Article in Metabolic brain disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Integrating Inflammatory and Epigenetic Signatures in IBD-Associated Colorectal Carcinogenesis: Models, Mechanisms, and Clinical Implications.International journal of molecular sciences · 2025Review
- The Multifaceted Roles of BACH1 in Disease: Implications for Biological Functions and Therapeutic Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Exosomes and non-coding RNAs in the regulation of neuroinflammation after ischemic stroke: mechanisms and therapeutic perspectives.Frontiers in immunology · 2025Review
- Circ_0008146 Exacerbates Ferroptosis via Regulating the miR-342-5p/ACSL4 Axis After Cerebral Ischemic/Reperfusion.Journal of inflammation research · 2024Article
- Long Non-Coding RNAs and Their "Discrete" Contribution to IBD and Johne's Disease-What Stands out in the Current Picture? A Comprehensive Review.International journal of molecular sciences · 2023Review
Corrections and comments
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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
backgroundCircular RNAs (circRNA) have been reported to be involved in the progression of cerebral infarction. The purpose of this study was to reveal the role and potential molecular mechanism of circZfp609 (mmu_circ_0001797) in cerebral infarction.
methodsC57BL/6J mice was used to construct middle cerebral artery occlusion (MCAO) mice model, and primary mouse astrocytes were treated with oxygen-glucose deprivation/reperfusion (OGD/R) process. The circZfp609, microRNA (miR)-145a-5p and BTB and CNC homology 1 (BACH1) expression levels were detected by quantitative real-time PCR. Cell proliferation and apoptosis were assessed by cell counting kit 8 assay, EdU assay and flow cytometry. Western blot analysis was used to measure protein levels, and ELISA assay was utilized to detect the levels of inflammation factors. Lactate dehydrogenase (LDH) level was measured by LDH Assay Kit. Dual-luciferase reporter assay, RIP assay and RNA pull-down assay were used to evaluate RNA interaction.
resultsCircZfp609 was upregulated in MCAO mice and OGD/R-induced astrocytes. Knockdown of circZfp609 promoted cell proliferation, while suppressed apoptosis and inflammation in OGD/R-induced astrocytes. CircZfp609 served as a sponge for miR-145a-5p, and miR-145a-5p inhibitor reversed the regulation of circZfp609 knockdown on OGD/R-induced astrocyte injury. BACH1 was a target of miR-145a-5p, and its overexpression abolished the inhibition effect of miR-145a-5p on OGD/R-induced astrocyte injury. Besides, circZfp609 downregulation also relieved the brain injury of MCAO mice through miR-145a-5p/BACH1 axis.
conclusionOur data showed that circZfp609 might promote cerebral infarction by regulating the miR-145a-5p/BACH1 pathway.
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