Potential of ferroptosis and ferritinophagy in migraine pathogenesis.

brain iron deposition ferritinophagy ferroptosis iron migraine migraine chronification periaqueductal gray

Journal

Frontiers in molecular neuroscience
ISSN: 1662-5099
Titre abrégé: Front Mol Neurosci
Pays: Switzerland
ID NLM: 101477914

Informations de publication

Date de publication:
2024
Historique:
received: 04 05 2024
accepted: 21 05 2024
medline: 25 6 2024
pubmed: 25 6 2024
entrez: 25 6 2024
Statut: epublish

Résumé

To assess the potential of ferroptosis and ferritinophagy in migraine pathogenesis. Ferroptosis and ferritinophagy are related to increased cellular iron concentration and have been associated with the pathogenesis of several neurological disorders, but their potential in migraine pathogenesis has not been explored. Increased iron deposits in some deep brain areas, mainly periaqueductal gray (PAG), are reported in migraine and they have been associated with the disease severity and chronification as well as poor response to antimigraine drugs. Iron deposits may interfere with antinociceptive signaling in the neuronal network in the brain areas affected by migraine, but their mechanistic role is unclear. Independently of the location, increased iron concentration may be related to ferroptosis and ferritinophagy in the cell. Therefore, both phenomena may be related to increased iron deposits in migraine. It is unclear whether these deposits are the reason, consequence, or just a correlate of migraine. Still, due to migraine-related elevated levels of iron, which is a prerequisite of ferroptosis and ferritinophagy, the potential of both phenomena in migraine should be explored. If the iron deposits matter in migraine pathogenesis, they should be mechanically linked with the clinical picture of the disease. As iron is an exogenous essential trace element, it is provided to the human body solely with diet or supplements. Therefore, exploring the role of iron in migraine pathogenesis may help to determine the potential role of iron-rich/poor dietary products as migraine triggers or relievers. Ferroptosis and ferritinophagy may be related to migraine pathogenesis through iron deposits in the deep areas of the brain.

Sections du résumé

Objective UNASSIGNED
To assess the potential of ferroptosis and ferritinophagy in migraine pathogenesis.
Background UNASSIGNED
Ferroptosis and ferritinophagy are related to increased cellular iron concentration and have been associated with the pathogenesis of several neurological disorders, but their potential in migraine pathogenesis has not been explored. Increased iron deposits in some deep brain areas, mainly periaqueductal gray (PAG), are reported in migraine and they have been associated with the disease severity and chronification as well as poor response to antimigraine drugs.
Results UNASSIGNED
Iron deposits may interfere with antinociceptive signaling in the neuronal network in the brain areas affected by migraine, but their mechanistic role is unclear. Independently of the location, increased iron concentration may be related to ferroptosis and ferritinophagy in the cell. Therefore, both phenomena may be related to increased iron deposits in migraine. It is unclear whether these deposits are the reason, consequence, or just a correlate of migraine. Still, due to migraine-related elevated levels of iron, which is a prerequisite of ferroptosis and ferritinophagy, the potential of both phenomena in migraine should be explored. If the iron deposits matter in migraine pathogenesis, they should be mechanically linked with the clinical picture of the disease. As iron is an exogenous essential trace element, it is provided to the human body solely with diet or supplements. Therefore, exploring the role of iron in migraine pathogenesis may help to determine the potential role of iron-rich/poor dietary products as migraine triggers or relievers.
Conclusion UNASSIGNED
Ferroptosis and ferritinophagy may be related to migraine pathogenesis through iron deposits in the deep areas of the brain.

Identifiants

pubmed: 38915936
doi: 10.3389/fnmol.2024.1427815
pmc: PMC11195014
doi:

Types de publication

Journal Article Review

Langues

eng

Pagination

1427815

Informations de copyright

Copyright © 2024 Fila, Przyslo, Derwich, Luniewska-Bury, Pawlowska and Blasiak.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Auteurs

Michal Fila (M)

Department of Developmental Neurology and Epileptology, Polish Mother's Memorial Hospital Research Institute, Lodz, Poland.

Lukasz Przyslo (L)

Department of Developmental Neurology and Epileptology, Polish Mother's Memorial Hospital Research Institute, Lodz, Poland.

Marcin Derwich (M)

Department of Developmental Dentistry, Medical University of Lodz, Lodz, Poland.

Jolanta Luniewska-Bury (J)

Faculty of Medicine, Collegium Medicum, Mazovian Academy in Plock, Plock, Poland.

Elzbieta Pawlowska (E)

Department of Developmental Dentistry, Medical University of Lodz, Lodz, Poland.

Janusz Blasiak (J)

Faculty of Medicine, Collegium Medicum, Mazovian Academy in Plock, Plock, Poland.

Classifications MeSH