Evidence map›Paper›PMID 42871048›Full record

ArticleFrontiers in cell and developmental biology2026

Integrated re-analysis of bulk and single-cell transcriptomic data reveals limited ferroptosis and neuroinflammation signatures after sevoflurane exposure in the aged rat hippocampus and human prefrontal cortex cells.

Zhenrong Zhang, Chen Hu, Yan Liu, Qin Zhang, Jiafei Liu, Zhihua Sun

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Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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6 authors.

Zhenrong Zhang *Department of Anesthesiology, Ninghai First Hospital, Ningbo, Zhejiang, China.
Chen Hu *Department of Anesthesiology, Huai'an Clinical Medical College of Jiangsu University (Huai'an Hospital of Huai'an City), Huai'an, Jiangsu, China.
Yan LiuDepartment of Anesthesiology, the 961st Hospital of the Joint Logistics Support Force of the Chinese People's Liberation Army, Qiqihar, Heilongjiang, China.
Qin ZhangDepartment of Anesthesiology, Ninghai First Hospital, Ningbo, Zhejiang, China.
Jiafei LiuDepartment of Anesthesiology, Ninghai First Hospital, Ningbo, Zhejiang, China.
Zhihua SunDepartment of Anesthesiology, Xiangya Hospital, Central South University, Changsha, Hunan, China.

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6 · The paper itself

Abstract

Background: Experimental studies have implicated ferroptosis in sevoflurane-associated neural injury, but the consistency of this signal across transcriptomic systems, species, and neural cell types remains uncertain. We therefore reassessed whether publicly available transcriptomic datasets support a coherent ferroptosis and neuroinflammation signature after sevoflurane exposure. Methods: We re-analysed two public transcriptomic datasets: GSE141242, comprising hippocampal tissue from aged rats exposed to 2.5% sevoflurane for 4 h (n = 3) or oxygen control (n = 3), and GSE196239, comprising human embryonic prefrontal cortex mixed-cell cultures exposed to sevoflurane, propofol, recovery conditions, or untreated control (one library per condition). After quality control, 67,272 single cells were retained. Bulk differential expression was assessed with an empirical-Bayes linear model, whereas the unreplicated single-cell conditions were summarized descriptively using key-gene expression, predefined gene-set scores, and observed cell-type composition. In addition, qRT-PCR was performed in C6 glioma cells and HA astrocytes assigned to Control, 3.3% sevoflurane for 6 h, H Results: In the aged-rat hippocampus, no probe set reached FDR < 0.05 (minimum FDR = 0.071), and the two groups did not separate clearly in principal-component space. In the human prefrontal cortex cultures, selected ferroptosis-related genes showed only small descriptive differences between the single control and sevoflurane libraries, and predefined gene-set summaries were likewise similar. Observed cell-type proportions differed by less than two percentage points, and no broad cell type showed a coherent sevoflurane-associated ferroptosis or inflammation pattern. The datasets were compared qualitatively rather than by formal cross-species correlation because of their marked biological and replication differences. In the four-group qRT-PCR experiment, sevoflurane and H Conclusion: The available public transcriptomic data do not provide robust evidence for a coordinated ferroptosis or neuroinflammation program attributable to sevoflurane across the examined systems. The four-group experiment showed that sevoflurane and H

Indexed as

ferroptosishippocampusneuroinflammationoxidative stressprefrontal cortexsevofluranesingle-cell RNA sequencingtranscriptomics

Identifiers

PMID42871048
PMCPMC13658196

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