ArticleBrain : a journal of neurology2021
Acute and non-resolving inflammation associate with oxidative injury after human spinal cord injury.
Article in Brain : a journal of neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
128 citing papers in PubMed, 3 syntheses or guidelines pooled it, 200 citations in OpenAlex.
- Multimodal microglial and kynurenine pathway alterations across the affective-psychosis spectrum: a systematic review of patterns, heterogeneity, and dimensional implications.Molecular psychiatry · 2026Pooled it
- Neuroprotective effect and possible mechanism of edaravone in rat models of spinal cord injury: a systematic review and network meta-analysis.Frontiers in pharmacology · 2025Pooled it
- Astaxanthin promotes locomotor function recovery and attenuates tissue damage in rats following spinal cord injury: a systematic review and trial sequential analysis.Frontiers in neuroscience · 2023Pooled it
- Lipid droplets as redox-active organelles after spinal cord injury: lipid peroxidation, mitochondrial dysfunction, and neuroinflammation.Redox report : communications in free radical research · 2026Review
- Hierarchical targeting biomimetic nanoparticles directing to lesion site and mitochondria promote neuroregeneration and attenuate inflammation after spinal cord injury.Materials today. Bio · 2026Article
- A BSCB-Penetrating Nanoplatform for Enhanced Luteolin Delivery in PRMT2-Targeted Epigenetic Therapy of Spinal Cord Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Notch Signaling in Spinal Cord Injury: Mechanistic Insights and Therapeutic Perspectives.Molecular neurobiology · 2026Review
- Cell-type-specific m1A dynamics are associated with microglial phenotypic transition and neuronal metabolic adaptation during spinal cord injury.PLoS computational biology · 2026Article
- Research on GM1 bound bMSCs loaded with SF hydrogel for spinal cord injury repair.Journal of translational medicine · 2026Article
- Integrating bulk and single-cell transcriptome profiling to uncover diagnostic biomarkers and regulatory mechanisms of oxidative stress in spinal cord injury.Neural regeneration research · 2026Article
- LPC18:0 Secreted by Exogenous Neural Stem Cells Potentiates Neurogenesis and Functional Recovery via GPR55-Mediated Signalling in Spinal Cord Injury.Cell proliferation · 2026Article
- Extracellular matrix remodelling in neurological diseases.Nature reviews. Neurology · 2026Review
- The Fidelity Paradox in Spinal Cord Injury: Reframing Biomechanical Mimicry and Neurobiological Relevance for Clinical Translation.CNS neuroscience & therapeutics · 2026Review
- Enhanced MIF/CD74 axis activity shapes B cell functioning following traumatic spinal cord injury.Journal of neuroinflammation · 2026Article
- Polydatin for treating spinal cord injury: Multiple mechanisms and challenges.Journal of pharmaceutical analysis · 2026Review
- Research Progress on Spinal Cord Repair Based on Regulation of the Neuroregenerative Microenvironment.Cellular and molecular neurobiology · 2026Review
- CREB5 Inhibits Neuronal Ferroptosis via Transactivating ApoL6 to Regulate Lipid Droplet Metabolism After Spinal Cord Injury.CNS neuroscience & therapeutics · 2026Article
- Spatiotemporal delivery of multifunctional nanozymes for neuroinflammation alleviation via autophagy modulation in spinal cord injury.Materials today. Bio · 2026Article
- NEDD4 promotes reactive astrogliosis by enhancing K63-linked ubiquitination and inhibiting chaperone-mediated autophagy degradation of YAP1.International journal of biological sciences · 2026Article
- The Role of MicroRNAs in Treg-Derived Extracellular Vesicles: A Narrative Review Focusing on Immune-Related Diseases.Journal of immunology research · 2026Review
68 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Traumatic spinal cord injury is a devastating insult followed by progressive cord atrophy and neurodegeneration. Dysregulated or non-resolving inflammatory processes can disturb neuronal homeostasis and drive neurodegeneration. Here, we provide an in-depth characterization of innate and adaptive inflammatory responses as well as oxidative tissue injury in human traumatic spinal cord injury lesions compared to non-traumatic control cords. In the lesion core, microglia were rapidly lost while intermediate (co-expressing pro- as well as anti-inflammatory molecules) blood-borne macrophages dominated. In contrast, in the surrounding rim, TMEM119+ microglia numbers were maintained through local proliferation and demonstrated a predominantly pro-inflammatory phenotype. Lymphocyte numbers were low and mainly consisted of CD8+ T cells. Only in a subpopulation of patients, CD138+/IgG+ plasma cells were detected, which could serve as candidate cellular sources for a developing humoral immunity. Oxidative neuronal cell body and axonal injury was visualized by intracellular accumulation of amyloid precursor protein (APP) and oxidized phospholipids (e06) and occurred early within the lesion core and declined over time. In contrast, within the surrounding rim, pronounced APP+/e06+ axon-dendritic injury of neurons was detected, which remained significantly elevated up to months/years, thus providing mechanistic evidence for ongoing neuronal damage long after initial trauma. Dynamic and sustained neurotoxicity after human spinal cord injury might be a substantial contributor to (i) an impaired response to rehabilitation; (ii) overall failure of recovery; or (iii) late loss of recovered function (neuro-worsening/degeneration).
Indexed as
Identifiers
What OpenQuestion holds
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.