ArticleThe Journal of experimental medicine2021
Normalization of cholesterol metabolism in spinal microglia alleviates neuropathic pain.
Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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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
58 citing papers in PubMed, 98 citations in OpenAlex.
- Glial cells in neuropathic pain.Physiological reviews · 2026Review
- Lipid Metabolism in Central Nervous System Diseases: Pathological Mechanisms and Therapeutic Advances.CNS neuroscience & therapeutics · 2026Review
- Article
- IRAK-M attenuates pain hypersensitivity and anxiety-like behaviors in a nitroglycerin-induced chronic migraine mouse model with concomitant reductions in microglial activation and neuroinflammation.The journal of headache and pain · 2026Article
- Lipid metabolism, microglia, and stroke.Neural regeneration research · 2026Article
- Lymphotoxin-beta receptor controls the development of chronic pain.Cell reports · 2026Article
- Article
- C-1101 multi-protein platelet and plasma-derived therapeutic to treat chronic lumbosacral radiculopathy.Frontiers in bioengineering and biotechnology · 2026Article
- FOXA2 regulated by HDAC3-mediated deacetylation attenuates neuropathic pain by modulating microglial lipid metabolism and synaptic pruning dysregulation.Journal of neuroinflammation · 2025Article
- Transcriptional regulation of disease-relevant microglial activation programs.bioRxiv : the preprint server for biology · 2025Article
- Progressive Loss of Astrocytic AIBP Expression during Alzheimer's Disease Pathology.bioRxiv : the preprint server for biology · 2025Article
- Restoring AIBP expression in the retina provides neuroprotection in glaucoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Pattern recognition receptors: function, regulation and therapeutic potential.Signal transduction and targeted therapy · 2025Review
- The Role of APOA-I in Alzheimer's Disease: Bridging Peripheral Tissues and the Central Nervous System.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Amyloid β-Induced Inflammarafts in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Cholesterol metabolism and neuroinflammatory changes in a non-human primate spinal nerve ligation model.Scientific reports · 2025Article
- The Integrated Transcriptome Bioinformatics Analysis of Energy Metabolism-Related Profiles for Dorsal Root Ganglion of Neuropathic Pain.Molecular neurobiology · 2025Article
- Monocytes across life span in HIV infection: lights and shadows.Current opinion in HIV and AIDS · 2025Review
- Article
- Innate immunity in chemotherapy-induced peripheral neuropathy: recent advances.Frontiers in pain research (Lausanne, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
21 authors at 2 institutions in 1 country.
Funding
Abstract
Neuroinflammation is a major component in the transition to and perpetuation of neuropathic pain states. Spinal neuroinflammation involves activation of TLR4, localized to enlarged, cholesterol-enriched lipid rafts, designated here as inflammarafts. Conditional deletion of cholesterol transporters ABCA1 and ABCG1 in microglia, leading to inflammaraft formation, induced tactile allodynia in naive mice. The apoA-I binding protein (AIBP) facilitated cholesterol depletion from inflammarafts and reversed neuropathic pain in a model of chemotherapy-induced peripheral neuropathy (CIPN) in wild-type mice, but AIBP failed to reverse allodynia in mice with ABCA1/ABCG1-deficient microglia, suggesting a cholesterol-dependent mechanism. An AIBP mutant lacking the TLR4-binding domain did not bind microglia or reverse CIPN allodynia. The long-lasting therapeutic effect of a single AIBP dose in CIPN was associated with anti-inflammatory and cholesterol metabolism reprogramming and reduced accumulation of lipid droplets in microglia. These results suggest a cholesterol-driven mechanism of regulation of neuropathic pain by controlling the TLR4 inflammarafts and gene expression program in microglia and blocking the perpetuation of neuroinflammation.
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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.