ReviewCureus2025
The Impact of Nuclear Factor Kappa B on the Response of Microglia in Spinal Cord Injuries.
Review in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Prenatal and Lactation Exposure to Bisphenol A (BPA) at the Global Mean Daily Intake Level Leads to Sex-Dependent Changes in Microglial State, Gene Expression, and Behavioral Patterns in Newborn and Juvenile Wistar Rat Offspring.Life (Basel, Switzerland) · 2026Article
- Transcriptomic analysis of the physiological responses to injuries induced accompanying intracortical microelectrode implantation.Biomaterials · 2026Article
- RNA Interference and Its Key Targets for Spinal Cord Injury Therapy: What Is Known So Far?International journal of molecular sciences · 2025Review
- The neuroinflammatory triumvirate: NF-κB, NLRP3, and mTOR in spinal cord injury.Inflammopharmacology · 2025Review
- Liposomal ellagic acid enhances the regenerative potential of ADMSC-laden nanofibrous PCL scaffolds in a rat model of spinal cord injury.Scientific reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) results in both primary and secondary damage, each contributing to the overall injury and its consequences. Following SCI, microglia, the resident immune cells of the central nervous system (CNS), undergo a series of complex responses that contribute to the pathophysiology of the injury. In the context of SCI, nuclear factor kappa B (NF-kB) emerged as a critical mediator in the regulation of inflammatory responses following SCI. The aim of this review is to provide a comprehensive understanding of the involvement of NF-kB in the response of microglia following SCI. The PUBMED database was searched using the following keywords: NF-kB AND microglia AND spinal cord injury. Clinical and experimental studies evaluating the role of NF-kB in the response of microglia following SCI were included. Systematic reviews, case reports, research protocols, conference articles, and studies in languages other than English were excluded. The final analysis included 52 studies. NF-kB signaling exerts profound effects on the microglial response following SCI, influencing the inflammatory milieu, tissue damage, and potential for repair and recovery. Deactivation of the NF-kB signaling pathway suppresses the production of proinflammatory mediators in microglia, after SCI. Moreover, NF-kB suppression has neuroprotective effects, as it mitigates neuronal apoptosis and facilitates the M2 microglial phenotype, alleviating tissue damage after SCI. Moreover, several microRNAs play a crucial role in regulating gene expression post-transcriptionally and have emerged as key regulators in microglia activation after SCI. Overall, the role of NF-kB in the response of microglia to SCI is complex and context-dependent. While NF-kB activation is involved in initiating and propagating the inflammatory response following SCI, it also plays a role in tissue repair and regeneration. Thus, modulating NF-kB signaling in microglia represents a potential therapeutic target for attenuating inflammation and promoting neuroprotection and tissue repair in SCI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.