Ferroptosis associated with secondary brain damage induced by hypertensive underlying biological processes in intracerebral hemorrhage and therapeutic prospects.

Patients with hemorrhagic stroke face high rates of mortality and long-term disability. Only approximately 25% of intracerebral hemorrhage (ICH) survivors regain the ability to live independently within six months after onset. Primary brain injury results not only from direct mechanical compression by the hematoma but also from tissue destruction occurring at the time of hemorrhage. Secondary injury is driven by neuroinflammation and oxidative stress triggered by erythrocyte lysis-derived products such as hemoglobin and iron ions. Ferroptosis, a form of regulated cell death first described by Dixon et al. in 2012, has been increasingly implicated in the pathogenesis of secondary brain injury (SBI) after ICH. Accumulating preclinical evidence demonstrates that ferroptosis contributes significantly to SBI, and although several ferroptosis-targeting agents have shown efficacy in experimental models, their clinical translation requires further validation.This review summarizes mechanisms through which ferroptosis influences neuronal damage, neuroinflammation, and blood-brain barrier disruption following ICH, and discusses ferroptosis-based therapeutic strategies that may provide new perspectives for ICH treatment.