Single-Cell RNA Sequencing Reveals Microglial Heterogeneity and Functional States After Cerebral Ischemia-Reperfusion Injury

Our study demonstrates that cerebral ischemia induces transcriptionally and functionally distinct microglial subpopulations, characterized by metabolic reprogramming and proinflammatory activation. ATF3 serves as a central regulator linking CH25H-mediated metabolic changes to cytokine-driven neuroinflammation, highlighting potential therapeutic targets for modulating microglial responses and mitigating ischemia-induced brain injury.

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Publication Details

Journal
Journal of Inflammation Research
Published
2025-12-01
DOI
https://doi.org/10.2147/jir.s539404
Citations
4
Primary Topic
Neuroinflammation and Neurodegeneration Mechanisms
Type
article
Field-Weighted Citation Impact
3.37
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article

Single-Cell RNA Sequencing Reveals Microglial Heterogeneity and Functional States After Cerebral Ischemia-Reperfusion Injury

Ruohan Sun, Shirong Wen, Bo Pan, Changda Qu et al.
4 citations
Journal of Inflammation Research
Neuroinflammation and Neurodegeneration Mechanisms
3.37
article

Single-Cell RNA Sequencing Reveals Microglial Heterogeneity and Functional States After Cerebral Ischemia-Reperfusion Injury

Ruohan Sun, Shirong Wen, Bo Pan, Changda Qu, Yushi Tang, Yujun Pan, Yewei Qu, Qi Zhang, Shanshan Shi, Fangqin Li, Yi Lian
article en
4 citations

Abstract

Our study demonstrates that cerebral ischemia induces transcriptionally and functionally distinct microglial subpopulations, characterized by metabolic reprogramming and proinflammatory activation. ATF3 serves as a central regulator linking CH25H-mediated metabolic changes to cytokine-driven neuroinflammation, highlighting potential therapeutic targets for modulating microglial responses and mitigating ischemia-induced brain injury.

Journal of Inflammation ResearchVol. Volume 18
Harbin Medical University (CN), Heilongjiang Provincial Hospital (CN), First Affiliated Hospital of Harbin Medical University (CN)
Openalex Percentile: Top 7%
Neuroinflammation and Neurodegeneration Mechanisms
3.37
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