ReviewFrontiers in immunology2025
Regulatory effect of inflammatory mediators in spinal cord injury.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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Who cites it
4 citing papers in PubMed.
- Modulation of p38 MAPK signaling in spinal cord injury by curcumin: targeting inflammation, oxidative stress, and apoptosis.Inflammopharmacology · 2026Review
- The "Double-Edged Sword" of Neutrophils in Trauma: From Pathophysiological Mechanisms to Precision Immunomodulation Strategies.International journal of molecular sciences · 2026Review
- Multiomics Profiling Identifies Tlr4 as a Therapeutic Target of Necroptosis in Spinal Cord Injury.Mediators of inflammation · 2026Article
- Exosomal miR-149 from human umbilical cord mesenchymal stem cells attenuates spinal cord injury-induced blood-spinal cord barrier disruption by suppressing the ET-1/PI3K/Akt signaling pathway.Stem cell research & therapy · 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) is a severe disabling central nervous system injury that can lead to severe sensory and motor dysfunction, and even paralysis. Depending on the mechanism of injury, SCI can be divided into primary injury and secondary injury. While secondary injury is the most critical stage in the pathophysiological process of SCI, which is the uncontrolled destructive cascade that follows. At present, symptoms are mainly alleviated and endogenous repair mechanisms are improved through drug intervention, surgical decompression and rehabilitation therapy, but they cannot directly promote nerve regeneration and functional recovery. Recently, an increasing number of studies have shown that the inflammatory response is a core link in secondary injury and plays a crucial role in regulating the pathological progression of acute and chronic SCI. Inflammatory mediators are key participants in the inflammatory response, which can trigger various neuropathological conditions and neurological dysfunction and are related to the severity of the injury. They are being explored as potential therapeutic targets for SCI and related diseases. Therefore, reducing the production of pro-inflammatory mediators is feasible and will also become a research hotspot in the future. This article summarizes the main sources of inflammatory mediators related to injury, their expression regulation, the key signaling pathways that regulate their production (such as Toll-like receptors, NF-κB, MAPK pathways, etc.), and their impact on the pathophysiology of SCI. In addition, treatment methods such as chemical antagonists, plant extracts and hormone therapy have been introduced to inhibit the expression of inflammatory mediators in order to control and improve the inflammatory microenvironment. This article mainly relies on preclinical research evidence to deeply analyze the core position of inflammatory mediators, providing a theoretical basis and direction guidance for the development of more effective SCI anti-inflammatory treatments.
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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 Socratic graph.