{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Li Y"],"funding":["General Program of the China Postdoctoral Science Foundation","WV-INBRE","General Program of the Heilongjiang Provincial Postdoctoral Science Foundation","Young Talents Program of the First Affiliated Hospital of Harbin Medical University","Natural Science Foundation of Heilongjiang Province","WV-CTSI","NIGMS NIH HHS"],"pagination":["119"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12870926"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(1)"],"pubmed_abstract":["Subarachnoid hemorrhage (SAH) is a devastating stroke subtype often leading to poor neurological outcomes. Iron homeostasis imbalance is a key contributor to cognitive dysfunction in neurological diseases. Extracellular vesicles, including exosomes (EXs), are crucial mediators of intercellular communication. This study investigated the role of EXs in post-SAH iron metabolism and neurological impairment. We isolated EXs from various neural cells (microglia, astrocytes, endothelial cells, neurons; n = 4-6 independent isolations) in vitro after SAH mimicked by oxyhemoglobin (OxyHb) or hemin. We found that microglial EXs (MC-EXs) were significantly enriched in iron and potently impaired neuronal viability. Using specific inhibitors and fluorescence imaging, we demonstrated that neurons interna"],"journal":["Journal of nanobiotechnology"],"pubmed_title":["Microglia-derived iron-overloaded exosomes induce neuronal ferroptosis and aggravate neurological impairment after subarachnoid hemorrhage."],"pmcid":["PMC12870926"],"funding_grant_id":["YQ2023H008","2021Y10","P20GM103434","2021MD703829","P20 GM103434","U54GM104942","LBH-Z20169","PL2024H055","U54 GM104942"],"pubmed_authors":["Meng F","Li X","Li Y","Yao Z","Chen J","Sun B","Wang XA","Wu P","Huang L","Bihl J","Shi H","Sawant H"],"additional_accession":[]},"is_claimable":false,"name":"Microglia-derived iron-overloaded exosomes induce neuronal ferroptosis and aggravate neurological impairment after subarachnoid hemorrhage.","description":"Subarachnoid hemorrhage (SAH) is a devastating stroke subtype often leading to poor neurological outcomes. Iron homeostasis imbalance is a key contributor to cognitive dysfunction in neurological diseases. Extracellular vesicles, including exosomes (EXs), are crucial mediators of intercellular communication. This study investigated the role of EXs in post-SAH iron metabolism and neurological impairment. We isolated EXs from various neural cells (microglia, astrocytes, endothelial cells, neurons; n = 4-6 independent isolations) in vitro after SAH mimicked by oxyhemoglobin (OxyHb) or hemin. We found that microglial EXs (MC-EXs) were significantly enriched in iron and potently impaired neuronal viability. Using specific inhibitors and fluorescence imaging, we demonstrated that neurons interna","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-07-15T06:11:28.451Z","creation":"2026-06-30T03:16:19.766Z"},"accession":"S-EPMC12870926","cross_references":{"pubmed":["41508018"],"doi":["10.1186/s12951-025-03974-y"]}}