ArticleNature communications2022
The alarmin interleukin-1α triggers secondary degeneration through reactive astrocytes and endothelium after spinal cord injury.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 60 citations in OpenAlex.
- A BSCB-Penetrating Nanoplatform for Enhanced Luteolin Delivery in PRMT2-Targeted Epigenetic Therapy of Spinal Cord Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Research on GM1 bound bMSCs loaded with SF hydrogel for spinal cord injury repair.Journal of translational medicine · 2026Article
- IL-1β-mediated interaction between Müller cells and microglia through CXCL1/5-CXCR2 aggravates visual dysfunction in experimental glaucoma.Journal of neuroinflammation · 2026Article
- Dual-targeting nanoparticles enhance microglial P2Y12R expression to promote neuronal mitophagy for repairing spinal cord injury.Cell death & disease · 2026Article
- Orchestrating neuroinflammation: A symphony of Interleukin-1 and cell type-specific Interleukin-1 receptor type 1 signaling in the brain.Brain behavior and immunity integrative · 2026Article
- Polydatin for treating spinal cord injury: Multiple mechanisms and challenges.Journal of pharmaceutical analysis · 2026Review
- TIA1-mediated stress granules inhibit the neuroinflammation and neurodegeneration after spinal cord injury through LCN2 signaling.Cellular and molecular life sciences : CMLS · 2026Article
- RPS3-Enriched Extracellular Vesicles Mediate Liver-Spinal Cord Inter-Organ Communication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- An interpretable machine learning model integrating early immune biomarkers for predicting outcomes after spinal cord injury.Frontiers in neurology · 2026Article
- Amyloid-Frontiers in neuroscience · 2026Review
- Glycolysis-related gene signatures in spinal cord injury pathophysiology identification through integrative gene expression analysis.Frontiers in genetics · 2026Article
- IL1A enhances TNF-induced retinal ganglion cell death.Frontiers in aging neuroscience · 2026Article
- Mitochondrial complex III-derived ROS amplify immunometabolic changes in astrocytes and promote dementia pathology.Nature metabolism · 2025Article
- Modeling Pain Without Injury: Inherited Rodent Models as Mechanistic Windows into Chronic Pain.Function (Oxford, England) · 2025Review
- IL-1α Promotes Cancer Cell Migration and Is a Potential Prognostic Marker in Oral Squamous Cell Carcinoma.Cancers · 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
- Neuroimmune signaling mediates astrocytic nucleocytoplasmic disruptions and stress granule formation associated with TDP-43 pathology.Neurobiology of disease · 2025Article
- Tanshinone IIA Promotes Functional Recovery After Spinal Cord Injury by Inhibiting Neuron and Oligodendrocyte Ferroptosis Through the GPX4/ACSL4 Axis.Neurochemical research · 2025Article
- Hydroxysafflower yellow A alleviates the inflammatory response in astrocytes following cerebral ischemia by inhibiting the LCN2/STAT3 feedback loop.Metabolic brain disease · 2025Article
- Single-Cell Multi-omics Assessment of Spinal Cord Injury Blocking via Cerium-doped Upconversion Antioxidant Nanoenzymes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 3 countries.
Funding
Abstract
Spinal cord injury (SCI) triggers neuroinflammation, and subsequently secondary degeneration and oligodendrocyte (OL) death. We report that the alarmin interleukin (IL)-1α is produced by damaged microglia after SCI. Intra-cisterna magna injection of IL-1α in mice rapidly induces neutrophil infiltration and OL death throughout the spinal cord, mimicking the injury cascade seen in SCI sites. These effects are abolished through co-treatment with the IL-1R1 antagonist anakinra, as well as in IL-1R1-knockout mice which demonstrate enhanced locomotor recovery after SCI. Conditional restoration of IL-1R1 expression in astrocytes or endothelial cells (ECs), but not in OLs or microglia, restores IL-1α-induced effects, while astrocyte- or EC-specific Il1r1 deletion reduces OL loss. Conditioned medium derived from IL-1α-stimulated astrocytes results in toxicity for OLs; further, IL-1α-stimulated astrocytes generate reactive oxygen species (ROS), and blocking ROS production in IL-1α-treated or SCI mice prevented OL loss. Thus, after SCI, microglia release IL-1α, inducing astrocyte- and EC-mediated OL degeneration.
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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.