ArticleMedComm2025
Integrative Multiomics Profiling of Mouse Hippocampus Reveals Transcriptional Upregulation of Interferon-Stimulated Genes Through PU.1 Regulator in Microglial Activation Induced by Chronic Cerebral Hypoperfusion.
Article in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Neuromodulation Techniques in Chronic Cerebral Hypoperfusion: Mechanisms and Therapeutic Advances.CNS neuroscience & therapeutics · 2026Review
- The CEBPB-AP-1 (JunB/Fos) Axis Drives Neuroinflammation and Microglial Dysfunction Via TNF Signaling in Ischemic Stroke.Inflammation · 2026Article
- Inhibition of Astrocytic JMJD3 Attenuates Neuroinflammation-Mediated Blood-Brain Barrier Disruption and Improves Functional Recovery After Intracerebral Hemorrhage in Mice.Brain sciences · 2026Article
- Flipping the Switch: MeCP2-Mediated Lactylation Rewires Microglial Metabolism and Inflammation via the HK2/mTOR Axis in Poststroke Neuroinflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Temporal Evolution of Brain Inflammation in the Bilateral Common Carotid Artery Stenosis Model of Chronic Cerebral Hypoperfusion.Journal of inflammation research · 2026Review
- hUMSC-Exosomes suppress TREM1-p38 MAPK signaling via HMGB1-dependent mechanisms to reprogram microglial function and promote neuroprotection in ischemic stroke.Journal of nanobiotechnology · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic cerebral hypoperfusion (CCH) is a significant factor that accelerates cognitive deterioration, yet the mechanisms of hippocampal microglial activation in this context remain unclear. Using an integrative multiomics approach, we investigated the transcriptional and epigenomic landscape of microglial activation in a mouse model of CCH induced by bilateral common carotid artery stenosis. Behavioral assessments revealed cognitive impairments, while neuropathological analysis confirmed hippocampal damage. Proteomic and transcriptomic profiling uncovered significant upregulation of stress and inflammatory pathways, particularly the interferon (IFN) signaling cascade. Epigenomic analysis identified regions of open chromatin, suggesting active transcriptional regulation driven by the transcription factor (TF) PU.1. ChIP-nexus analysis further confirmed that PU.1 directly modulates the expression of IFN-stimulated genes (ISGs), which are pivotal in regulating microglial activation. Our findings demonstrate that PU.1 serves as a key regulator of the IFN-driven microglial response during CCH, mediated by enhanced chromatin accessibility and transcriptional activation of ISGs. This study highlights the critical role of PU.1 in microglial-mediated neuroinflammation and offers potential therapeutic targets for mitigating hippocampal damage associated with chronic cerebral ischemia.
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Registered trials
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