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Updated: May 3, 2026

The Rabbit Blood-shunt Model for the Study of Acute and Late Sequelae of Subarachnoid Hemorrhage: Technical Aspects
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Ferroptosis mechanisms in early brain injury after subarachnoid hemorrhage

Wanying Du1, Junhui Chen1, Gefei Cheng1

  • 1Department of Neurosurgery, 904th Hospital of Joint Logistic Support Force of PLA, Wuxi Clinical College of Anhui Medical University, Wuxi 214044, China.

Brain Research
|March 9, 2026
PubMed

Subarachnoid hemorrhage (SAH) refers to the rupture of intracranial blood vessels, leading to blood entering the subarachnoid space. It is primarily caused by the rupture of intracranial aneurysms and represents a severe acute cerebrovascular disease. Early brain injury (EBI) denotes the pathological changes occurring within 72 h after SAH, including increased intracranial pressure, reduced cerebral blood flow, blood-brain barrier disruption, brain edema, oxidative stress, and neuroinflammation. Ferroptosis is an iron-dependent form of programmed cell death (PCD), and its mechanisms can be summarized into three interrelated aspects: iron metabolism, lipid peroxidation metabolism, and glutathione and amino acid metabolism. Recent studies indicate that ferroptosis is associated with EBI and is significantly correlated with a poor prognosis. This article reviews the latest research progress on ferroptosis in early brain injury after subarachnoid hemorrhage and provides new insights for future research.

Keywords:
EarlybraininjuryFerroptosisMechanismOxidative stressSubarachnoidhemorrhage

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