Evidence map›Paper›PMID 41403939›Full record

ArticleFrontiers in immunology2025

Altered lipid profiles in the prefrontal cortex are associated with neuroinflammation after severe burn injury.

Sean O'Leary, Anesh Prasai, Ariadna Robledo, Christopher Thang, Ye Wang, Rahul R Deshpande, William K Russell, Andrew J Murton, Steven E Wolf, Amina El Ayadi

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Sean O'LearyDepartment of Neurosurgery, University of Texas Medical Branch, Galveston, TX, United States.
Anesh PrasaiDepartment of Surgery, University of Texas Medical Branch, Galveston, TX, United States.
Ariadna RobledoDepartment of Medicine, University of Miami, Miami, FL, United States.
Christopher ThangDepartment of Dermatology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States.
Ye WangDepartment of Surgery, University of Texas Medical Branch, Galveston, TX, United States.
Rahul R DeshpandeDepartment of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX, United States.
William K RussellDepartment of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX, United States.
Andrew J MurtonDepartment of Surgery, University of Texas Medical Branch, Galveston, TX, United States.
Steven E WolfDepartment of Surgery, University of Texas Medical Branch, Galveston, TX, United States.
Amina El AyadiDepartment of Surgery, University of Texas Medical Branch, Galveston, TX, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Severe burn injuries can cause long-term cognitive impairments, potentially driven by lipid-mediated neuroinflammation in the central nervous system (CNS). The disruption of lipid homeostasis may contribute to neuroinflammatory responses, exacerbating neuronal damage. This study investigates whether acipimox, an anti-lipolytic agent, modulates lipid accumulation and neuroinflammation in the prefrontal cortex following severe burns. Methods: Sprague Dawley rats were randomized into four groups: sham vehicle, sham acipimox, burn vehicle, and burn acipimox. A scald injury covering 40-60% of total body surface area was induced, and rats were treated with acipimox (50 mg/kg/day, intraperitoneally) or vehicle for seven days. Lipidomic analysis assessed alterations in lipid profiles, while machine learning (XGBoost) identified key lipid drivers of burn-induced neuroinflammation. Additionally, mRNA expression of inflammatory markers, including interleukin-1β (IL-1β), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and toll-like receptor 4 (TLR4), was quantified to evaluate neuroinflammatory responses. Cytokine-lipid correlations were also examined using Spearman analysis. Results: Lipidomic analysis identified significant alterations in a subset of the 21 lipid classes analyzed, particularly long-chain and very-long-chain fatty acids, including lysophosphatidylethanolamines, lysophosphatidylcholines, phosphatidylglycerols, phosphatidylethanolamines, and triacylglycerols ( Discussion: These findings suggest that severe burns induce significant lipid dysregulation in the CNS, contributing to neuroinflammation and potential cognitive impairment. By targeting lipolysis, acipimox mitigates lipid accumulation, suppresses inflammatory pathways, and normalizes lipid levels, highlighting a potential therapeutic mechanism. Conclusion: This study establishes a mechanistic link between elevated lipolysis and CNS inflammation following severe burns. Acipimox effectively modulates lipid profiles and reduces neuroinflammation, underscoring its potential for managing burn-induced neurological complications. Further studies are needed to validate these findings and explore clinical applications.

Indexed as

BurnsLipid MetabolismLipidsNeuroinflammatory DiseasesPrefrontal CortexAnimalsCytokinesDisease Models, AnimalLipidomicsMaleNF-kappa BRatsRats, Sprague-DawleyToll-Like Receptor 4CytokinesLipidsNF-kappa BToll-Like Receptor 4acipimoxburn injurycytokineslipidomicslipolysismachine learningneuroinflammationprefrontal cortex

Identifiers

PMID41403939
PMCPMC12702713

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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.