Evidence map›Paper›PMID 40636749›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2025

Assessing the developmental effects of fentanyl and impacts on lipidomic profiling using neural stem cell models.

Cheng Wang, Jinchun Sun, Rohini Donakonda, Richard Beger, Leah E Latham, Leihong Wu, Shuliang Liu, Joseph P Hanig, Fang Liu

Abstract read
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 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. 2024 international conference on neuroprotective agents conference proceedings.Experimental biology and medicine (Maywood, N.J.) · 2025
    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

9 authors.

Cheng Wang *Division of Neurotoxicology, National Center for Toxicological Research/FDA, Jefferson, AR, United States.
Jinchun Sun *Division of Systems Biology, National Center for Toxicological Research/U.S. Food and Drug Administration (FDA), Jefferson, AR, United States.
Rohini DonakondaDivision of Systems Biology, National Center for Toxicological Research/U.S. Food and Drug Administration (FDA), Jefferson, AR, United States.
Richard BegerDivision of Systems Biology, National Center for Toxicological Research/U.S. Food and Drug Administration (FDA), Jefferson, AR, United States.
Leah E LathamDivision of Neurotoxicology, National Center for Toxicological Research/FDA, Jefferson, AR, United States.
Leihong WuDivision of Bioinformatics and Biostatistics, National Center for Toxicological Research/FDA, Jefferson, AR, United States.
Shuliang LiuDivision of Neurotoxicology, National Center for Toxicological Research/FDA, Jefferson, AR, United States.
Joseph P HanigOffice of Pharmaceutical Quality, Center for Drug Evaluation and Research/U.S. Food and Drug Administration (FDA), Silver Spring, MD, United States.
Fang LiuDivision of Neurotoxicology, National Center for Toxicological Research/FDA, Jefferson, AR, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fentanyl is a potent and short-acting opioid that is often given to pediatric patients during surgery to relieve pain and as an adjunct to anesthesia. Its effects on the developing brain are yet to be determined. In the present study, commercially available human neural stem cells (NSCs) were used to model the effects of fentanyl on the developing human brain. We determined the dose dependent effects and temporal relationships between fentanyl exposures and NSC health, viability, and differentiation. Markers of mitochondrial health [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetra-zolium bromide (MTT)] and cell death/damage [lactate dehydrogenase (LDH)] were monitored to determine the dose response effects of fentanyl on NSC viability. In addition, lipidomics analysis was conducted to investigate lipid profile changes in differentiated neural cells treated with fentanyl. Fentanyl did not cause a significant increase in LDH release, nor MTT reduction after 24-h exposure at concentrations of 0.5, 1.0, 3.0, 10, or 100 μM, for both NSCs and differentiated neural cells. Lipidomics data showed the top 15 most variable important in projection (VIP) lipid species (the higher the VIP scores, the bigger changes in treated groups vs. controls), including lysophosphatidylcholines (LPCs), lysophosphatidylethanolamines (LPEs), ceramides (CER), cholesterol esters (ChEs) and sphingosine (SPH). The lipidomic data indicate that LPC (16:0), LPC (16:1), LPC (18:1), CER (d18:0_22:0), CER (d18:2_18:0), CER(d18:2_24:1) were significantly increased, and only ChE (24:5) and SPH (d18:1) were significantly decreased in the highest dose group versus control. These data indicated that fentanyl exposure (24-h) did not induce detectable cell death. However, a lipidomic analysis indicated that fentanyl may affect immature neural cell functions through modifying lipid composition and lipid metabolism. These data indicated that despite the absence of clear neurodegeneration, fentanyl may still have a negative impact on the developing brain.

Indexed as

Analgesics, OpioidFentanylLipid MetabolismLipidomicsNeural Stem CellsCell DifferentiationCell SurvivalHumansAnalgesics, OpioidFentanylanestheticsdevelopmentfentanyllipidomic analysisneurotoxicity

Identifiers

PMID40636749
PMCPMC12237720

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Registered trials

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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.