ArticleNature communications2024
NAAA-regulated lipid signaling in monocytes controls the induction of hyperalgesic priming in mice.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- The endocannabinoid 2-arachidonoylglycerol mediates seasonal life-history transitions in a wild reptile.The Journal of experimental biology · 2026Article
- Article
- Peripheral Blood Cells and Clinical Profiles as Biomarkers for Pain Detection in Palliative Care Patients.Biomedicines · 2026Article
- Polyethylene terephthalate microplastics exposure enhances the risk of ulcerative colitis: insights from multiomics integration, machine learning, and molecular docking reveal intestinal toxicity mechanisms.International journal of surgery (London, England) · 2026Article
- Metabolic reprogramming in the spinal cord drives the transition to pain chronicity.Cell reports · 2025Article
- Neuroprotective, anti-inflammatory, and analgesic activity of palmitoylethanolamide in sickle cell mice.Blood advances · 2025Article
- Metabolic reprogramming in the spinal cord drives the transition to pain chronicity.bioRxiv : the preprint server for biology · 2025Article
- Targeting microglial NAAA-regulated PEA signaling counters inflammatory damage and symptom progression of post-stroke anxiety.Cell communication and signaling : CCS · 2025Article
- N-acylethanolamine acid amidase inhibitor-loaded polymeric micelles in the treatment of dry eye disease.International journal of ophthalmology · 2025Article
- ΔThe Journal of pharmacology and experimental therapeutics · 2024Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Circulating monocytes participate in pain chronification but the molecular events that cause their deployment are unclear. Using a mouse model of hyperalgesic priming (HP), we show that monocytes enable progression to pain chronicity through a mechanism that requires transient activation of the hydrolase, N-acylethanolamine acid amidase (NAAA), and the consequent suppression of NAAA-regulated lipid signaling at peroxisome proliferator-activated receptor-α (PPAR-α). Inhibiting NAAA in the 72 hours following administration of a priming stimulus prevented HP. This effect was phenocopied by NAAA deletion and depended on PPAR-α recruitment. Mice lacking NAAA in CD11b
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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.