ArticleNature neuroscience2019
Microvascular endothelial cells engulf myelin debris and promote macrophage recruitment and fibrosis after neural injury.
Article in Nature neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers.
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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.
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Who cites it
151 citing papers in PubMed, 239 citations in OpenAlex.
- Lipid droplets as redox-active organelles after spinal cord injury: lipid peroxidation, mitochondrial dysfunction, and neuroinflammation.Redox report : communications in free radical research · 2026Review
- Artificial hibernation: A new technique for protecting neural tissue and organs.Neural regeneration research · 2026Article
- Neonatal small extracellular vesicle-loaded GelNB hydrogel reprograms the vascular-immune microenvironment for spinal cord injury repair.Bioactive materials · 2026Article
- Single-cell RNA sequencing of the post-spinal cord injury dorsal root ganglia in cynomolgus monkeys: Elucidation of the cellular immune microenvironment of the central nervous system.Neural regeneration research · 2026Article
- Upregulation of the Mitophagy-Related Gene EXOSC4 Is Associated with Immune Dysregulation in Spinal Cord Injury.Molecular neurobiology · 2026Article
- ABCA1-mediated lipid efflux restrains oxidative stress and neuroinflammation after spinal cord injury.Journal of neuroinflammation · 2026Article
- Phagocytosis is crucial for brain repair.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Article
- TGF-β-induced fibrotic scar formation limits recovery of spinal cord injury.Bone research · 2026Article
- TREM2 Facilitates Myelin Debris Clearance but Exacerbates Chronic Inflammation and Fibrosis After Spinal Cord Injury.CNS neuroscience & therapeutics · 2026Article
- Surface Charge-Determined Protein Coronas of Nanoparticles Control Endothelial Cells Uptake Under Low Magnitude Shear Stress.Exploration (Beijing, China) · 2026Article
- A Conjugation Delivery System of Macrophages and Platelet Pharmacytes Promotes Regeneration After Spinal Cord Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Progress on Omega-3 fatty acids for the comprehensive and targeted treatment of spinal cord injury.Bone research · 2026Review
- Astrocytic Sirt2-Mediated Delactylation Limits Blood-Spinal Cord Barrier Reconstruction after Spinal Cord Injury.Research (Washington, D.C.) · 2026Article
- Type 2 Diabetes Promotes the Microglial Pyroptosis by Activating NLRP3 Inflammasome to Impede Remyelination After Spinal Cord Injury.Research (Washington, D.C.) · 2026Article
- Targeting angiogenesis and white matter repair for enhanced functional recovery after acute ischemic stroke: A focus on the roles of glial cells.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Decoding autophagy in neuro-tumor crosstalk: from underlying mechanisms to translational opportunities.Theranostics · 2026Review
- Article
- Repurposing of Chemokine Antagonists for Combined Phase-Resolved Spinal Cord Injury Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- TREML2 Modulates Microglial Phagocytosis of Myelin Debris via TLR9 in Chronic Cerebral Ischemia.Inflammation · 2025Article
- Brain-cervical lymph node crosstalk contributes to brain injury induced by subarachnoid hemorrhage in mice.Nature communications · 2025Article
91 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
20 authors at 8 institutions in 5 countries.
Funding
Abstract
The clearance of damaged myelin sheaths is critical to ensure functional recovery from neural injury. Here we show a previously unidentified role for microvessels and their lining endothelial cells in engulfing myelin debris in spinal cord injury (SCI) and experimental autoimmune encephalomyelitis (EAE). We demonstrate that IgG opsonization of myelin debris is required for its effective engulfment by endothelial cells and that the autophagy-lysosome pathway is crucial for degradation of engulfed myelin debris. We further show that endothelial cells exert critical functions beyond myelin clearance to promote progression of demyelination disorders by regulating macrophage infiltration, pathologic angiogenesis and fibrosis in both SCI and EAE. Unexpectedly, myelin debris engulfment induces endothelial-to-mesenchymal transition, a process that confers upon endothelial cells the ability to stimulate the endothelial-derived production of fibrotic components. Overall, our study demonstrates that the processing of myelin debris through the autophagy-lysosome pathway promotes inflammation and angiogenesis and may contribute to fibrotic scar formation.
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