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Erbin, a scaffold protein involved in multiple cellular signaling pathways, regulates neuroinflammation and may confer neuroprotection against ischemia\u2013reperfusion (I\/R) injury. A mouse model of middle cerebral artery occlusion was utilized to evaluate the neuroprotective role of Erbin. Male mice were allocated into groups receiving either a lentiviral (LV) control vector or LV-mediated Erbin overexpression, followed by I\/R injury induction. Neurological function, infarct volume, and expression levels of inflammatory cytokines and mitogen-activated protein kinase (MAPK) signaling proteins were analyzed. Overexpression of Erbin via LV transduction significantly reduced cerebral infarct volume and mitigated neurological impairments post-I\/R injury. Furthermore, Erbin overexpression suppressed the phosphorylation of p38 and extracellular signal-regulated kinase in HT22 neuronal cells, indicating attenuation of MAPK pathway activation. Notably, Erbin overexpression modulated the inflammatory response elicited by I\/R injury, leading to a reduction in proinflammatory cytokine levels.<\/jats:p>","DOI":"10.1523\/eneuro.0089-25.2026","type":"journal-article","created":{"date-parts":[[2026,4,27]],"date-time":"2026-04-27T17:50:18Z","timestamp":1777312218000},"page":"ENEURO.0089-25.2026","update-policy":"https:\/\/doi.org\/10.1523\/eneuro.crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Erbin Confers Neuroprotection against Cerebral Ischemia\u2013Reperfusion Injury in Mice via MAPK Pathway 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