ArticleiScience2025
Chemerin 15 enhances microglial phagocytosis to attenuate cerebral ischemia-reperfusion injury through the ChemR23/p38 MAPK pathway.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Immuno-resolving nitric oxide-generating stents for coordinated vascular healing.Bioactive materials · 2027Article
- Tissue-Specific Chemerin in Atherosclerosis.Biomolecules · 2026Review
- Protocol for studying Chemerin 15-enhanced microglial phagocytosis in cerebral ischemia-reperfusion injury via the ChemR23/p38 MAPK pathway.STAR protocols · 2026Article
- Inflammation-centered neurovascular-immune-metabolic remodeling in ischemic stroke: stage-dependent mechanisms, regulated cell death, and therapeutic translation.Frontiers in immunology · 2026Review
- Highly Alkaline-ResistantMicroorganisms · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglia recover and maintain homeostasis in the central nervous system by phagocytosing dead cells and harmful substances under pathological conditions. Chemerin 15 (C15), a chemerin-derived peptide, is an endogenous phagocytic and inflammatory regulator that acts via the G protein-coupled receptor, ChemR23. However, the effect of C15 on microglial phagocytosis following ischemia-reperfusion injury remains unclear. Here, we found that microglial phagocytosis was activated and dynamically altered after ischemia-reperfusion injury. C15 administration promoted microglial phagocytosis of bioparticles and neuronal debris and upregulated the phagocytosis-related genes and pathways. Furthermore, C15 binding to ChemR23 decreased damage-associated molecular patterns (DAMPs) and ROS production and further alleviated the infarct volume and neurological deficits after ischemia-reperfusion injury. Thus, C15 is a potential therapeutic target for the recovery of neurological function after stroke.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.