ArticleNeurobiology of disease2024
PI3K signaling promotes formation of lipid-laden foamy macrophages at the spinal cord injury site.
Article in Neurobiology of disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 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
- Elevated phagocytic capacity directs innate spinal cord repair.Cell reports · 2026Article
- The role of autophagy in spinal cord injury: Mechanisms, crosstalk, and therapeutic strategies.Neural regeneration research · 2026Article
- Structural and functional evolution of IL-1 targeting: From systemic neutralization to bioengineered nanotherapies.Materials today. Bio · 2026Review
- SARM1 is required for macrophage immunophenotype switching that is essential for nerve repair.bioRxiv : the preprint server for biology · 2026Article
- Mitochondrial metabolism restoration via Tramiprosate suppresses mitochondrial ROS-driven foamy macrophage senescence post spinal cord injury.Journal of orthopaedic translation · 2026Article
- Phagocytosis and neuroinflammation: orchestrating central nervous system homeostasis, repair, and the resolution of inflammation.Trends in neurosciences · 2026Review
- AXL Promotes Ischemic Myelin Repair Through Alleviating Myelin Debris Deposition and Lipid Droplets Accumulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Lipid accumulation in foam cells drives C1q-dependent synaptic loss and impairs motor function recovery after spinal cord injury.Communications biology · 2025Article
- A Myelin Debris Cleaner for Spinal Cord Injury Recovery: Polycaprolactone / Cell Membrane Assembled Scaffolds.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Molecular pathology of acute spinal cord injury in middle-aged mice.Journal of neuroinflammation · 2025Article
- The protective PLCγ2-P522R variant mitigates Alzheimer's disease-associated pathologies by enhancing beneficial microglial functions.Journal of neuroinflammation · 2025Article
- Nitroxidative Stress, Cell-Signaling Pathways, and Manganese Porphyrins: Therapeutic Potential in Neuropathic Pain.International journal of molecular sciences · 2025Review
- Microglia and programmed cell death in spinal cord injury: beyond apoptosis.Frontiers in cell and developmental biology · 2025Review
- A review focuses on a neglected and controversial component of SCI: myelin debris.Frontiers in immunology · 2024Review
- Biomaterials targeting the microenvironment for spinal cord injury repair: progression and perspectives.Frontiers in cellular neuroscience · 2024Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
After spinal cord injury (SCI), infiltrating macrophages undergo excessive phagocytosis of myelin and cellular debris, forming lipid-laden foamy macrophages. To understand their role in the cellular pathology of SCI, investigation of the foamy macrophage phenotype in vitro revealed a pro-inflammatory profile, increased reactive oxygen species (ROS) production, and mitochondrial dysfunction. Bioinformatic analysis identified PI3K as a regulator of inflammation in foamy macrophages, and inhibition of this pathway decreased their lipid content, inflammatory cytokines, and ROS production. Macrophage-specific inhibition of PI3K using liposomes significantly decreased foamy macrophages at the injury site after a mid-thoracic contusive SCI in mice. RNA sequencing and in vitro analysis of foamy macrophages revealed increased autophagy and decreased phagocytosis after PI3K inhibition as potential mechanisms for reduced lipid accumulation. Together, our data suggest that the formation of pro-inflammatory foamy macrophages after SCI is due to the activation of PI3K signaling, which increases phagocytosis and decreases autophagy.
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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.