ArticleCell & bioscience2025
CircRNA Itm2b induces oxidative stress via the interaction with Sirt1-Nox4 to aggravate sleep disturbances after traumatic brain injury.
Article in Cell & bioscience, 2025. 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 7 papers.
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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
7 citing papers in PubMed.
- Chasing the FoxO in Metabolic Disorders: Novel Considerations for Oxidative Stress, Programmed Cell Death, Wnt, and the Gut Microbiome.Antioxidants (Basel, Switzerland) · 2026Review
- Running out the clock: Circadian rhythm dysfunction in cognitive disease.International review of neurobiology · 2026Review
- Agitation, Alzheimer's disease, and autophagy: mechanistic insights into aging pathways, gut microbiome, and artificial intelligence.Frontiers in immunology · 2026Review
- CircRNA-Based Therapeutics: a New Frontier in Neuroinflammation Treatment.Molecular neurobiology · 2025Review
- Brain-derived extracellular vesicles circUsp32 polarized macrophages causing acute kidney injury after traumatic brain injury.Science advances · 2025Article
- Correction: CircRNA Itm2b induces oxidative stress via the interaction with Sirt1-Nox4 to aggravate sleep disturbances after traumatic brain injury.Cell & bioscience · 2025Article
- Anxiety and Depression: Triggers for Cognitive Loss, Alzheimer's Disease, and Neurodegeneration.Current neurovascular research · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
Abstract
Sleep disorders (SD) are common sequelae following traumatic brain injury (TBI) and may be linked to mitochondrial oxidative stress dysregulation after TBI. Increasing evidence showed that circRNAs play crucial roles in nervous system diseases. However, the involvement of circRNAs in sleep disturbances after TBI is not characterized. In this study, differentially expressed circRNAs were identified by RNA sequencing. Sleep quality in TBI patients was assessed through sleep scales and electroencephalograms. Further experiments were conducted to investigate the role of circItm2b. We found that circItm2b was elevated and involved sleep disorder in TBI patients. Over-expression of circItm2b might aggravate sleep disturbances in mice after TBI. Mechanically, circItm2b regulates Nox4 expression through binding Sirt1, which influences mitochondrial oxidative stress-caused circadian protein losses. Moreover, the knockdown of circItm2b attenuated mitochondrial oxidative stress-induced circadian proteins losses via circItm2b/Sirt1/Nox4 axis after TBI, which might suggest that circItm2b may serve as a prognostic marker for improving sleep disorders and represent a promising therapeutic target for TBI-related sleep disturbances.
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