Microglia-derived iron-overloaded exosomes induce neuronal ferroptosis and aggravate neurological impairment after subarachnoid hemorrhage.

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

SUBMITTER: Li Y 

PROVIDER: S-EPMC12870926 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature