Evidence map›Paper›PMID 41240164›Full record

ArticleMetabolic brain disease2025

Identification of hub genes and pathways associated with sevoflurane-induced synaptic loss in diabetic offspring via comprehensive transcriptome analysis.

Xiaoru Sun, Xinke Guo, Tingmei Wu, Weimin Tao, Rong Lin, Yujie Song, Yuhan Zheng, Changsheng Ma, Fuyi Shen, Yilu Zhou and 1 more

Abstract read
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Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
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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

11 authors.

Xiaoru Sun *Department of Anesthesiology, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, People's Republic of China.
Xinke Guo *Department of Anesthesiology, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, People's Republic of China.
Tingmei Wu *Department of Anesthesiology, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, People's Republic of China.
Weimin TaoDepartment of Anesthesiology, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, People's Republic of China.
Rong LinDepartment of Anesthesiology, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, People's Republic of China.
Yujie SongDepartment of Anesthesiology, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, People's Republic of China.
Yuhan ZhengDepartment of Anesthesiology, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, People's Republic of China.
Changsheng MaDepartment of Anesthesiology, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, People's Republic of China.
Fuyi ShenDepartment of Anesthesiology, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, People's Republic of China.
Yilu ZhouDepartment of Anesthesiology, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, People's Republic of China. zhouyilu@51mch.com.ORCID 0009-0002-7874-4176
Zhendong XuDepartment of Anesthesiology, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, People's Republic of China. btxzd123@51mch.com.ORCID 0000-0002-2696-3492

Funding

Health Industry Clinical Research Specialized Program of Shanghai Municipal Health Commission Grant No. 20224Y0068Shanghai Association of Chinese Integrative Medicine MT23-3
6 · The paper itself

Abstract

Vulnerable brain models exhibit heightened susceptibility to anesthetic neurotoxicity, with diabetic offspring warranting particular attention, yet the underlying mechanisms remain unclear. This study integrated bioinformatics and experiments to investigate the molecular basis of sevoflurane-induced neurodevelopmental toxicity in diabetic offspring. Offspring of streptozotocin-induced diabetic dams (gestational diabetes model) and control mice were exposed to sevoflurane (2.5%, 3 × 2 h, P6-P8). Hippocampal tissues underwent RNA sequencing. Bioinformatics analysis identified dysregulated pathways, followed by validation of neuronal apoptosis (TUNEL), synaptic proteins (PSD-95, Synaptophysin), and microglial activity (Iba1+). Hub genes were screened via protein-protein interaction networks. Diabetic-sevoflurane offspring showed aberrant activation of neural crest differentiation, oxidative stress/redox pathways, and microglial pathogen phagocytosis. Compare with the Control group the diabetic-sevoflurane offspring showed increased apoptosis, synaptic loss and enhanced Iba1 + microglial density. Uty, Uba1y, Ddx3y, Kdm5d, and Eif2s3y were identified as key regulators. Gestational diabetes primes microglia via Hub gene networks, amplifying sevoflurane-induced neurotoxicity. Targeting these genes may mitigate risks in diabetic offspring requiring anesthesia.Clinical trial number: Not applicable.

Indexed as

Anesthetics, InhalationDiabetes, GestationalDiabetes Mellitus, ExperimentalPrenatal Exposure Delayed EffectsSevofluraneSynapsesTranscriptomeAnimalsApoptosisFemaleGene Expression ProfilingGene Regulatory NetworksHippocampusMaleMiceMice, Inbred C57BLAnesthetics, InhalationSevofluraneAnestheticGestational diabetesMicrogliaNeuronNeurotoxicity

Identifiers

PMID41240164

What OpenQuestion holds

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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.