ArticleMolecular brain2025
Targeting CD74 in microglia to modulate experimental cerebral ischemia and reperfusion injury: insights from Single-Cell and bulk transcriptomics.
Article in Molecular brain, 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.
- Analytical Methods and Application of Single-Cell and Single-Nucleus Transcriptomics in the Study of Ischemic Stroke.Biomolecules · 2026Review
- Hyperbaric Oxygen Attenuates Cerebral Ischemia-Reperfusion Injury Through ROS-Dependent Remodeling of Microglial Mitochondrial Dynamics.International journal of molecular sciences · 2026Article
- A-to-I RNA editing profiles and distinct immune responses in myelin oligodendrocyte glycoprotein antibody-positive optic neuritis.Frontiers in immunology · 2026Article
- Single-cell and single-nucleus transcriptomics in ischemic stroke: cellular mechanisms and therapeutic implications.Frontiers in neurology · 2026Review
- Review
- Altered Neuroinflammatory Transcriptomic Profile in the Hippocampal Dentate Gyrus Three Weeks After Lateral Fluid Percussion Injury in Rats.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Ischemic stroke remains a leading cause of mortality and long-term disability, with reperfusion injury contributing significantly to poor clinical outcomes. Microglia, the primary immune cells of the central nervous system, play a dual role in ischemic stroke by both exacerbating injury through neuroinflammation and supporting recovery through neuroprotection. This study aimed to explore the role of CD74, a gene upregulated in microglia following ischemia-reperfusion injury. Using single-cell RNA sequencing and bulk RNA sequencing, we identified CD74 as a potential target involved in microglial-mediated neuroinflammation. We observed a significant increase in CD74 expression in microglia following middle cerebral artery occlusion/reperfusion (MCAO/R), which correlated with pro-inflammatory cytokine production and neuroinflammation. Targeted knockdown of CD74 in microglia using CX3CR1Cre/ERT2 mice led to a reduction in infarct volume, inflammatory cytokine levels, and long-term neurological deficits. Behavioral tests showed improved motor coordination, sensory function, and exploratory behavior in CD74 knockdown mice. These results suggest that CD74 is a critical mediator of microglia-driven neuroinflammation, and targeting CD74 may represent a promising therapeutic strategy for reducing ischemic brain injury and promoting recovery after stroke.
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Registered trials
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