ArticleJournal of neuroinflammation2023
A breakdown of metabolic reprogramming in microglia induced by CKLF1 exacerbates immune tolerance in ischemic stroke.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The trial behind it
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Microglia-targetedMaterials today. Bio · 2026Article
- CAR design equips diverse immune cells with unique antigen-specific activation identities.Molecular therapy. Oncology · 2026Article
- Microglial Immunometabolic Remodeling After Ischemic Stroke: The Interplay Between Mitochondrial Stress and the Ischemic Microenvironment.Translational stroke research · 2026Review
- Ginsenoside Rg1 alleviates post-ischemic stroke neuroinflammation by inhibiting CKLF1-mediated suppression of dead/dying neuron clearance.Acta pharmaceutica Sinica. B · 2026Article
- Mild hypothermia inhibits the inflammatory response and microglial M1 polarization in ischemic stroke via the EFNB2/EphB4 pathway.Metabolic brain disease · 2026Article
- Neuroinflammation after stroke: initiation, amplification and therapeutic prospects.Journal of translational medicine · 2026Review
- Immunotherapies for Ischemic Stroke Patients: Current Status and Future Directions.Medical sciences (Basel, Switzerland) · 2026Review
- Microglia Mitochondrial Metabolism in Neurological Diseases.Molecular neurobiology · 2026Review
- Inflammation-centered neurovascular-immune-metabolic remodeling in ischemic stroke: stage-dependent mechanisms, regulated cell death, and therapeutic translation.Frontiers in immunology · 2026Review
- Perioperative neurocognitive disorders as a neuroimmune landscape disorder: microglial priming, state heterogeneity, and time-dependent neuroinflammation.Frontiers in immunology · 2026Review
- The spatiotemporal dynamic evolution of post-stroke neuroinflammation: energy metabolism mechanisms of acute response and chronic progression.Frontiers in pharmacology · 2026Review
- The SARS-CoV-2 nucleocapsid protein induces microglia senescence-mediated cognitive impairment via Glycolysis.Molecular medicine (Cambridge, Mass.) · 2025Article
- Review
- Characterization of SPTLC2 as a key driver promoting microglial activation and energy metabolism reprogramming after ischemic stroke through bulk and single-cell analyses combined with experimental validation.Cell biology and toxicology · 2025Article
- Microglial Autophagy and Mitophagy in Ischemic Stroke: From Dual Roles to Therapeutic Modulation.Biology · 2025Review
- CKLF1 disrupts microglial efferocytosis following acute ischemic stroke by binding to phosphatidylserine.Cell death and differentiation · 2025Article
- Targeting and reprogramming microglial phagocytosis of neutrophils by ginsenoside Rg1 nanovesicles promotes stroke recovery.Bioactive materials · 2025Article
- Long-Term Minocycline Treatment Exhibits Enhanced Therapeutic Effects on Ischemic Stroke by Suppressing Inflammatory Phenotype of Microglia Through the EMB/MCT4/STING Pathway.CNS neuroscience & therapeutics · 2025Article
- Acupuncture Improves Chronic Cerebral Ischemia by Inhibiting the CKLF1/HIF-1α/VEGF/Notch1 Signaling Pathway.CNS neuroscience & therapeutics · 2025Article
- Examining the Impact of Microglia on Ischemic Stroke With an Emphasis on the Metabolism of Immune Cells.CNS neuroscience & therapeutics · 2025Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Ischemic stroke is characterized by the presence of reactive microglia. However, its precise involvement in stroke etiology is still unknown. We used metabolic profiling and showed that chemokine like factor 1 (CKLF1) causes acute microglial inflammation and metabolic reprogramming from oxidative phosphorylation to glycolysis, which was reliant on the AMP-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR)-hypoxia inducible factor 1α (HIF-1α) signaling pathway. Once activated, microglia enter a chronic tolerant state as a result of widespread energy metabolism abnormalities, which reduces immunological responses, including cytokine release and phagocytosis. Metabolically dysfunctional microglia were also found in mice using genome-wide RNA sequencing after chronic administration of CKLF1, and there was a decrease in the inflammatory response. Finally, we showed that the loss of CKLF1 reversed the defective immune response of microglia, as indicated by the maintenance its phagocytosis to neutrophils, thereby mitigating the long-term outcomes of ischemic stroke. Overall, CKLF1 plays a crucial role in the relationship between microglial metabolic status and immune function in stroke, which prepares a potential therapeutic strategy for ischemic stroke.
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Registered trials
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