Subarachnoid hemorrhage (SAH) is a neurosurgical emergency that can result in severe neurological deficits or even death.1,2 SAH occurs when there is bleeding into the subarachnoid space. Roughly 85% of nontraumatic SAH cases result from the rupture of aneurysms, while the remaining 15%–20% stem from a variety of causes, with the bleeding mechanism often proving elusive.3 Despite accounting for only 5% of all strokes, SAH has high rates of mortality and disability, and poor clinical outcomes place a significant burden on society and families.4

Despite advancements in medical care, patients with SAH still face a high risk of complications, including early and delayed injury.5,6 The sudden increase in intracranial pressure results in a significant drop in cerebral perfusion pressure and early ischemia.7, 8, 9 Further, delayed cerebral ischemia (DCI), occurring 3–4 days after the initial hemorrhage, leads to further neurologic deterioration.9,10 This DCI is associated with vasospasm as they often coincide with each other11 and is secondary to microthrombosis, neurovascular uncoupling, and inflammatory responses.9,10

Recent studies have suggested a potential link between ferroptosis, a type of programmed cell death caused by lipid peroxidation, and neural cell death following SAH. This article aims to review the current knowledge on the role of ferroptosis in SAH with a focus on delayed cerebral injuries, including vasospasm. Understanding the mechanisms underlying these pathologies may accelerate the development of targeted therapies for SAH.