Ferroptosis in Epilepsy: From Molecular Mechanisms to Possible Therapeutic Alternatives

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 72

Special Issue Editors


E-Mail Website
Guest Editor
Institute of Physiopathology and Clinical Biochemistry, Faculty of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina
Interests: ABC-transporters; refractory epilepsy; hypoxia; pharmacoresistance

E-Mail Website
Guest Editor
Institute of Physiopathology and Clinical Biochemistry, Faculty of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina
Interests: drug resistant epilepsy; cannabidiol; antiepileptic drugs

Special Issue Information

Dear Colleagues,

Ferroptosis, a type of cell death in which excess reactive oxygen species are catalyzed by iron, has recently emerged as a consequence of epileptic seizures. However, the molecular mechanisms through which seizures lead to ferroptosis have not been fully established. In this context, imbalances in the NRF transcription factor pathway and the groups of genes under its control appear to be involved in the seizure response. However, interactions with other pathways, such as the response to inflammation and/or hypoxia, have not yet been established. On the other hand, the physiological response to epileptic seizures may promote imbalances in iron metabolism, thereby triggering ferroptosis in the central nervous system. This interaction with peripheral organs and systems has been poorly investigated and could represent a pivotal axis on which therapeutic strategies to control ferroptosis levels in the brain parenchyma could work. One piece of physiological evidence of the ferroptosis process is the formation of hemosiderin, an insoluble iron precipitate, which has been clinically linked to the occurrence of epileptic seizures. The surgical removal of hemosiderin in cavernoma surgery is necessary to achieve complete seizure control.

Our aim for this Special Issue is to generate a transversal axis of evidence that connects the molecular mechanisms that determine the process of ferroptosis, its interaction with other molecular pathways involved in epilepsy, and its relationship with other physiological systems to possible new strategies for the control of epileptic seizures, especially those that are drug-resistant.

Prof. Dr. Alberto Lazarowski
Dr. Jerónimo Andrés Auzmendi
Guest Editors

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Keywords

  • epilepsy
  • ferroptosis
  • hypoxia
  • brain parenchyma
  • peripheral organs
  • iron metabolism
  • transferrin
  • hemosiderin

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