ArticleJournal of neuroinflammation2020
CCL3 contributes to secondary damage after spinal cord injury.
Article in Journal of neuroinflammation, 2020. 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 56 papers, 1 of them a synthesis that pooled it.
What it found
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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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- The cytokines interleukin-6 and interferon-α induce distinct microglia phenotypes.Journal of neuroinflammation · 2022Pooled it
- PIWIL2 drives stroke progression via modulation of NF-κB signaling.Molecular therapy. Nucleic acids · 2026Article
- L-Threonic Acid Inhibits Pathological Retinal Neovascularization by Modulation of CCL3-CCR5 Signaling Pathway.Investigative ophthalmology & visual science · 2026Article
- B4Galnt1 Deficiency Reverses Severe Neurological Symptoms in a Mouse Model of Tay-Sachs Disease.Neuromolecular medicine · 2026Article
- Repurposing of Chemokine Antagonists for Combined Phase-Resolved Spinal Cord Injury Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The ferroptosis-mediated domino effect: metabolic crosstalk from intervertebral disc degeneration to spinal deformity and cord injury: a mini review.Frontiers in neuroscience · 2026Review
- The heme-binding protein hemopexin promotes functional recovery and tissue protection after spinal cord injury via sex-specific regulation of inflammation and ferroptosis.Journal of neuroinflammation · 2025Article
- Inflammation increases the penetrance of behavioral impairment inbioRxiv : the preprint server for biology · 2025Article
- Degenerating intervertebral discs in the streptozotocin-high-fat diet model of type 2 diabetes show extensive inflammation.Disease models & mechanisms · 2025Article
- The transcriptome and secreted factors of the intervertebral discs in STZ-HFD Type 2 diabetic male mice reveal extensive inflammation.bioRxiv : the preprint server for biology · 2025Article
- F-box/LRR-repeat protein 12 reorchestrated microglia to inhibit scarring and achieve adult spinal cord injury repair.Signal transduction and targeted therapy · 2025Article
- Gene Expression Changes as Biomarkers of Immunosenescence in Bulgarian Individuals of Active Age.Biomedicines · 2025Article
- Formoterol alters chemokine expression and ameliorates pain behaviors after moderate spinal cord injury in female mice.The Journal of pharmacology and experimental therapeutics · 2025Article
- The Therapeutic Potential of MicroRNA-21 in the Treatment of Spinal Cord Injury.Current issues in molecular biology · 2025Review
- Unveiling the Temporal Dynamics and Molecular Regulation Profiles of Neutrophil Extracellular Traps Following Spinal Cord Injury.Journal of inflammation research · 2025Article
- Reduction of inflammatory biomarkers underlies extracellular vesicle mediated functional recovery in an aged monkey model of cortical injury.Frontiers in aging neuroscience · 2025Article
- Novel diagnostic biomarkers associated with macrophage-microglia in spinal cord injury.Frontiers in immunology · 2025Article
- The emerging role of cuproptosis in spinal cord injury.Frontiers in immunology · 2025Review
- Regulation of dynamic spatiotemporal inflammation by nanomaterials in spinal cord injury.Journal of nanobiotechnology · 2024Review
- Long-term follow-up of brain regional changes and the association with cognitive impairment in quarantined COVID-19 survivors.European archives of psychiatry and clinical neuroscience · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSecondary damage after spinal cord injury (SCI) is characterized by a cascade of events including hemorrhage, apoptosis, oxidative stress, and inflammation which increase the lesion size which can influence the functional impairment. Thus, identifying specific mechanisms attributed to secondary injury is critical in minimizing tissue damage and improving neurological outcome. In this work, we are investigating the role of CCL3 (macrophage inflammatory protein 1-α, MIP-1α), a chemokine involved in the recruitment of inflammatory cells, which plays an important role in inflammatory conditions of the central and peripheral nervous system.
methodsA mouse model of lower thoracic (T11) spinal cord contusion injury was used. We assessed expression levels of CCL3 and its receptors on the mRNA and protein level and analyzed changes in locomotor recovery and the inflammatory response in the injured spinal cord of wild-type and CCL3
resultsThe expression of CCL3 and its receptors was increased after thoracic contusion SCI in mice. We then examined the role of CCL3 after SCI and its direct influence on the inflammatory response, locomotor recovery and lesion size using CCL3
conclusionWe have identified CCL3 as a potential target to modulate the inflammatory response and secondary damage after SCI. Collectively, this study shows that CCL3 contributes to progressive tissue damage and functional impairment during secondary injury after SCI.
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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.