ArticleJournal of orthopaedic surgery and research2026
circ_0044235 exacerbates neuroinflammation and apoptosis following spinal cord injury by targeting miR-338-5p.
Article in Journal of orthopaedic surgery and research, 2026. 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 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Correction: circ_0044235 exacerbates neuroinflammation and apoptosis following spinal cord injury by targeting miR-338-5p.Journal of orthopaedic surgery and research · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
Abstract
backgroundSpinal cord injury (SCI) triggers a cascade of secondary damages, including neuroinflammation and apoptosis, which critically impede neurological recovery. This study aims to investigate the function of circ_0044235 in this pathological process.
methodsIn this study, an in vitro injury model was established by stimulating PC-12 cells with lipopolysaccharide (LPS), and an in vivo SCI model was prepared by the rat T9-10 percussion method. The recovery of motor function in rats was evaluated by BBB score. RT-qPCR was used to determine the levels of circ_0044235, miR-338-5p, and mRNA. Cell viability and apoptosis were detected by MTT and flow cytometry. ELISA was used to determine the levels of inflammatory factors. The interaction between circ_0044235 and miR-338-5p was verified by dual-luciferase reporter gene and RNA pull-down.
resultLPS treatment up-regulated circ_0044235 expression and exacerbated PC-12 cell injury in a concentration-dependent manner. Silencing circ_0044235 improved cell viability, suppressed apoptosis, and reduced inflammatory factor release. Mechanistically, circ_0044235 directly bound to and negatively regulated miR-338-5p, with rescue experiments confirming its pro-injury role via miR-338-5p sponging. In vivo, knockdown of circ_0044235 promoted motor function recovery and reduced inflammation; these effects were reversed by a miR-338-5p antagomir. LRP1 was further identified as a direct downstream target of miR-338-5p.
conclusioncirc_0044235 functions as a key pro-injury factor in SCI. It directly targets and adsorbs miR-338-5p, thereby exacerbating the neuroinflammatory response and the process of apoptosis, and ultimately hindering the recovery of neural function.
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