ArticleiScience2026
C3aR inhibition alleviates cerebral ischemia-reperfusion injury via STING-mediated ferroptosis through SLC7A11/GPX4.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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7 authors.
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Abstract
Cerebral ischemia-reperfusion injury couples complement activation with innate immune signaling and ferroptotic lipid peroxidation. We investigated whether C3aR signaling modulates stimulator of interferon genes (STING)-associated ferroptosis through the solute carrier family 7 member 11 (SLC7A11)/glutathione peroxidase 4 (GPX4) anti-ferroptotic pathway. In rat middle cerebral artery occlusion/reperfusion (MCAO/R) and BV2 oxygen-glucose deprivation/reperfusion (OGD/R) models, C3aR blockade with SB290157 was examined with 2'3'-cGAMP-mediated STING activation, immunofluorescence, western blotting, reverse transcription quantitative PCR (RT-qPCR), ferroptosis assays, and molecular docking, molecular dynamics (MD), and molecular mechanics/generalized Born surface area (MM/GBSA) analyses. C3aR inhibition improved neurological outcomes, limited infarction and edema, preserved mitochondrial membrane potential, reduced microglia-associated STING activation and ferroptosis-related Fe
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