2. Academic Validation
  3. Chemerin 15 enhances microglial phagocytosis to attenuate cerebral ischemia-reperfusion injury through the ChemR23/p38 MAPK pathway

Chemerin 15 enhances microglial phagocytosis to attenuate cerebral ischemia-reperfusion injury through the ChemR23/p38 MAPK pathway

  • iScience. 2025 Aug 19;28(9):113396. doi: 10.1016/j.isci.2025.113396.
Yuhan Yang 1 2 3,  Yan Huang 1 2,  Jun Li 1 2,  Kunyi Li 1 2,  Changhao Mao 1 4,  Gang Liu 1 4,  Shuang Li 1 2,  Lan Wen 1 2
Affiliations

Affiliations

  • 1 School of Clinical Medicine, Chengdu Medical College, Chengdu 610500, P.R. China.
  • 2 Department of Neurology, The First Affiliated Hospital of Chengdu Medical College, Chengdu 610500, P.R. China.
  • 3 Department of Neurology, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.
  • 4 Department of Neurosurgery, The First Affiliated Hospital of Chengdu Medical College, Chengdu 610500, P.R. China.
PMID: 40970195 DOI: 10.1016/j.isci.2025.113396
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.

Keywords

Cell biology; Molecular biology; Neuroscience; Pharmacology.

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