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Ferroptosis therapeutic modalities for glioblastoma: Molecular mechanisms, resistance reversal, and barrier overcoming
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DOI：10.1016/j.gendis.2026.102370.png)
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Abstract
En 中文
Ferroptosis is an iron-dependent regulated cell death modality driven by lipid peroxidation and is mechanistically distinct from apoptosis, necroptosis, and pyroptosis. Morphologically, ferroptosis is associated with mitochondrial alterations, including increased membrane density and condensed mitochondria. Targeting ferroptosis may provide therapeutic opportunities to address tumor heterogeneity and circumvent apoptosis resistance. Glioblastoma is a highly malignant, treatment-refractory brain tumor with a distinct metabolic state and oxidative-stress landscape, which may render it particularly susceptible to ferroptosis-based interventions. Standard-of-care therapy for glioblastoma comprises maximal safe resection followed by radiotherapy and temozolomide; however, durable efficacy is frequently limited by resistance to therapy-induced cell death. Therefore, identifying targets that reverse chemo- and radioresistance, together with developing delivery strategies that overcome the blood–brain barrier, is critical for improving therapeutic outcomes. Emerging evidence suggests that ferroptosis influences chemoresistance and radioresistance and may be leveraged to enhance targeted drug delivery. This review synthesizes recent advances in ferroptosis research in glioblastoma, with an emphasis on pathway regulation, autophagy-dependent ferroptosis mechanisms, approaches to overcome chemoradiation resistance, emerging therapeutics, and nanomedicine-based, blood–brain barrier-penetrant delivery strategies. We also discuss current challenges, knowledge gaps, and future directions for ferroptosis-based glioblastoma therapy.
Keywords:
Blood–brain barrier
Ferroptosis
Ferroautophagy
Molecular mechanism
Nanodelivery
Radiation resistance
Resistance reversal
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