ArticleAging2021
Circular RNA Plek promotes fibrogenic activation by regulating the miR-135b-5p/TGF-βR1 axis after spinal cord injury.
Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Targeting the glial-fibrotic scar microenvironment after spinal cord injury: From integrated protection to systematic regulation of regenerative balance.Journal of orthopaedic translation · 2026Review
- A neurological prognostic nomogram integrating biomarkers and clinical indicators for surgically treated patients with osteoporotic spinal fracture and spinal cord injury.Scientific reports · 2026Article
- Intraoperative shear wave elastography during surgical treatment of intramedullary spinal cord tumors.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026Article
- Inflammatory protein mediators linking gut microbiota to degenerative lumbar spine disorders: cross-disease genetic evidence.Frontiers in immunology · 2026Article
- Microglia-vascular interactions after spinal cord injury: regulatory mechanisms and therapeutic advances.Frontiers in immunology · 2026Review
- miR-135b: An emerging player in cardio-cerebrovascular diseases.Journal of pharmaceutical analysis · 2024Review
- The Role of Neuromodulation and Potential Mechanism in Regulating Heterotopic Ossification.Neurochemical research · 2024Review
- The roles of circular RNAs in nerve injury and repair.Frontiers in molecular neuroscience · 2024Review
- Recent Advances in the Treatment of Spinal Cord Injury.The archives of bone and joint surgery · 2024Review
- Identification and Validation of Ferroptosis-Related Genes in Patients with Acute Spinal Cord Injury.Molecular neurobiology · 2023Article
- Article
- Identification of a circRNA-mediated comprehensive ceRNA network in spinal cord injury pathogenesis.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Screening the immune-related circRNAs and genes in mice of spinal cord injury by RNA sequencing.Frontiers in immunology · 2022Article
- circ_014260/miR-384/THBS1 aggravates spinal cord injury in rats by promoting neuronal apoptosis and endoplasmic reticulum stress.American journal of translational research · 2022Article
- Empagliflozin protects diabetic pancreatic tissue from damage by inhibiting the activation of the NLRP3/caspase-1/GSDMD pathway in pancreatic β cells: in vitro and in vivo studies.Bioengineered · 2021Article
- Circ-Usp10 promotes microglial activation and induces neuronal death by targeting miRNA-152-5p/CD84.Bioengineered · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThe spinal cord rarely repairs itself when damaged; however, methods for encouraging nerves to regrow are on the horizon. Although circular RNAs (circRNAs) contribute to various biological processes, including neuronal processes, their functions in the subacute phase of spinal cord injury (SCI) have not been elucidated. In this study, we identified a novel circRNA, named CircPlek, with increased expression in spinal tissues after SCI. MATERIALS AND
methodsWe predicted a regulatory relationship between CircPlek and miR-135b-5p, which showed the most obvious decrease in post-SCI expression. We established the CircPlek/miR-135b-5p/transforming growth factor-beta receptor type I (TGF-βR1) axis using a bioinformatics approach and further evaluated the potential function of the interaction network
resultsWe confirmed that in TGF-β1-induced fibroblasts, the overexpression of miR-135b-5p or/and inhibition of CircPlek inhibited fibrosis activation via the Smad pathway. Inhibitors of miR-135b-5p had antagonistic effects on CircPlek.
conclusionsthe CircPlek/miR-135b-5p/TGF-βR1 axis may exert important functions in SCI and is a potential therapeutic target.
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