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We investigated whether ferroptosis contributes to acute ischemic stroke using a transient middle cerebral artery occlusion model in pial collateral-deficient CB-17\/Icr-+\/+Jcl mice. Mice were subjected to 90\u2009min of ischemia followed by reperfusion, and the effects of the ferroptosis inhibitor UAMC-3203 on infarct evolution and post-stroke histological changes were examined. UAMC-3203 increased the survival of CD13-positive pericytes within infarct areas and enhanced infarct reduction in the subacute phase. In vitro, the glutathione peroxidase 4 inhibitor RAS-selective lethal 3 (RSL3) induced dose-dependent cell death in pericytes but not in endothelial cells, which was suppressed by UAMC-3203 but not by inhibitors of apoptosis or necroptosis. RSL3 induced lipid peroxidation in pericytes, as evidenced by malondialdehyde accumulation. Extracellular ferrous iron (Fe\n                    <jats:sup>2+<\/jats:sup>\n                    ), but not ferric iron (Fe\n                    <jats:sup>3+<\/jats:sup>\n                    ) or transferrin, caused intracellular Fe\n                    <jats:sup>2+<\/jats:sup>\n                    accumulation and cell death in pericytes, which was further enhanced by oxygen\u2013glucose deprivation with reperfusion and suppressed by UAMC-3203. Myelin debris containing abundant Fe\n                    <jats:sup>2+<\/jats:sup>\n                    induced ferroptosis in cultured pericytes. These findings indicate that pericytes are a major ferroptosis-vulnerable cell type during ischemia\u2013reperfusion and may represent a therapeutic target in acute ischemic stroke.\n                  <\/jats:p>","DOI":"10.1177\/0271678x261463955","type":"journal-article","created":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T05:18:22Z","timestamp":1783315102000},"page":"2697-2710","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":1,"title":["Ferroptosis of microvascular pericytes contributes to ischemia\u2013reperfusion injury in mice"],"prefix":"10.1177","volume":"46","author":[{"given":"Hayato","family":"Takaki","sequence":"first","affiliation":[{"name":"Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 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