Oxidative Imbalance as an Amplifier of Migraine Pathophysiology

Valeria Magnelli^*, Davide Rotondo
Department of Science and Technological Innovation, University of Piemonte Orientale “Amedeo Avogadro”, Alessandria, Italy
* Corresponding Author: Valeria Magnelli. Email: email

BIOCELL https://doi.org/10.32604/biocell.2026.084728

Received 28 April 2026; Accepted 09 September 2026; Published online 15 September 2026

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Abstract

Migraine is a prevalent neurovascular disorder characterized by recurrent unilateral headaches, nausea, and hypersensitivity to environmental stimuli. Despite its multifactorial pathophysiology, a definitive mechanism underlying its pathogenesis remains elusive. Increasing evidence implicates oxidative stress (OS) as a contributing factor, driven by the overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) arising from mitochondrial dysfunction, neuronal hyperexcitability, and inflammation. Experimental animal models have shown that ROS and RNS target cellular and molecular components, including nociceptive receptors, vascular endothelial cells, mitochondria, and ion channels. Clinical studies in migraine patients further support this link, demonstrating elevated oxidative damage markers alongside reduced antioxidant defenses. A major unresolved question is whether OS acts primarily as an amplifier of existing pathological processes or as a driver of disease onset and progression. This review aims to delineate the role of OS within the migraine pathological network, focusing on its cellular and molecular targets and the potential downstream consequences. Elucidating OS-modulated pathways may provide a foundation for developing innovative therapeutic strategies for migraine and related pain disorders.