ArticleExperimental neurology2014
CD36 deletion improves recovery from spinal cord injury.
Article in Experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Endoplasmic Reticulum Stress in Spinal Cord Injury: Pathological Roles, Molecular Targets, and Emerging Treatments: A Systematic Review.Molecular neurobiology · 2026Pooled it
- Multifaceted Immune Effects of the Scavenger Receptor CD36 on Long-Term Outcomes After Neonatal Arterial Focal Stroke.Journal of neurochemistry · 2026Article
- APOE-mediated lipid transport prevents C1q-related synaptic loss after spinal cord injury via attenuating macrophage lipid stress.Journal of neuroinflammation · 2026Article
- Mitochondrial metabolism restoration via Tramiprosate suppresses mitochondrial ROS-driven foamy macrophage senescence post spinal cord injury.Journal of orthopaedic translation · 2026Article
- Inhibition of CD36 ameliorates mouse spinal cord injury by accelerating microglial lipophagy.Acta pharmacologica Sinica · 2025Article
- Interleukin-3 Modulates Macrophage Phagocytic Activity and Promotes Spinal Cord Injury Repair.CNS neuroscience & therapeutics · 2024Article
- CD36 deletion prevents white matter injury by modulating microglia polarization through the Traf5-MAPK signal pathway.Journal of neuroinflammation · 2024Article
- CHAC1: a master regulator of oxidative stress and ferroptosis in human diseases and cancers.Frontiers in cell and developmental biology · 2024Review
- Targeting transcription factor pu.1 for improving neurologic outcomes after spinal cord injury.Frontiers in neuroscience · 2024Article
- The role of foam cells in spinal cord injury: challenges and opportunities for intervention.Frontiers in immunology · 2024Review
- Enhanced oxidative phosphorylation, re-organized intracellular signaling, and epigenetic de-silencing as revealed by oligodendrocyte translatome analysis after contusive spinal cord injury.Scientific reports · 2023Article
- Identification of Ferroptotic Genes in Spinal Cord Injury at Different Time Points: Bioinformatics and Experimental Validation.Molecular neurobiology · 2022Article
- Myelin and non-myelin debris contribute to foamy macrophage formation after spinal cord injury.Neurobiology of disease · 2022Article
- Taurolithocholic acid but not tauroursodeoxycholic acid rescues phagocytosis activity of bone marrow-derived macrophages under inflammatory stress.Journal of cellular physiology · 2022Article
- Limited changes in locomotor recovery and unaffected white matter sparing after spinal cord contusion at different times of day.PloS one · 2021Article
- Improved locomotor recovery after contusive spinal cord injury in Bmal1Scientific reports · 2020Article
- Reduced FAK-STAT3 signaling contributes to ER stress-induced mitochondrial dysfunction and death in endothelial cells.Cellular signalling · 2017Article
- Macrophage Transcriptional Profile Identifies Lipid Catabolic Pathways That Can Be Therapeutically Targeted after Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Building an RNA Sequencing Transcriptome of the Central Nervous System.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2016Review
- Inflammogenesis of Secondary Spinal Cord Injury.Frontiers in cellular neuroscience · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
CD36 is a pleiotropic receptor involved in several pathophysiological conditions, including cerebral ischemia, neurovascular dysfunction and atherosclerosis, and recent reports implicate its involvement in the endoplasmic reticulum stress response (ERSR). We hypothesized that CD36 signaling contributes to the inflammation and microvascular dysfunction following spinal cord injury. Following contusive injury, CD36(-/-) mice demonstrated improved hindlimb functional recovery and greater white matter sparing than CD36(+/+) mice. CD36(-/-) mice exhibited a reduced macrophage, but not neutrophil, infiltration into the injury epicenter. Fewer infiltrating macrophages were either apoptotic or positive for the ERSR marker, phospho-ATF4. CD36(-/-) mice also exhibited significant improvements in injury heterodomain vascularity and function. These microvessels accumulated less of the oxidized lipid product 4-hydroxy-trans-2-nonenal (4HNE) and exhibited a reduced ERSR, as detected by vascular phospho-ATF4, CHOP and CHAC-1 expression. In cultured primary endothelial cells, deletion of CD36 diminished 4HNE-induced phospho-ATF4 and CHOP expression. A reduction in phospho-eIF2α and subsequent increase in KDEL-positive, ER-localized proteins suggest that 4HNE-CD36 signaling facilitates the detection of misfolded proteins upstream of eIF2α phosphorylation, ultimately leading to CHOP-induced apoptosis. We conclude that CD36 deletion modestly, but significantly, improves functional recovery from spinal cord injury by enhancing vascular function and reducing macrophage infiltration. These phenotypes may, in part, stem from reduced ER stress-induced cell death within endothelial and macrophage cells following injury.
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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.