[Research progress on mitochondrial genetic mechanisms underlying the onset of migraine]

Migraine is a common primary headache disorder in clinical practice, and its recurrent nature severely impairs patients' quality of life. Data from the 2021 Global Burden of Disease Study indicate that migraine imposes a heavy burden on patients, their families, and society. In recent years, the association between mitochondrial dysfunction and migraine has attracted increasing attention. Studies have demonstrated that during migraine attacks, skeletal muscle cells exhibit significant mitochondrial morphological changes (such as mitochondrial swelling and cristae disruption), while platelets show mitochondrial biochemical abnormalities (e.g., reduced respiratory chain enzyme activity). Impaired energy metabolism in the brain tissue of migraine patients suggests that mitochondrial dysfunction may be involved in the pathogenesis of migraine. With rapid advances in technologies such as high-throughput sequencing and targeted sequencing, genetic variations in mitochondrial DNA (mtDNA) have gradually become a research hotspot in the etiology of migraine. Several studies have identified mtDNA genetic variations in migraine patients, which may affect the onset and progression of migraine by regulating mitochondrial energy metabolism pathways and inducing oxidative stress. This article systematically summarizes recent research progress on the correlation between migraine and mtDNA, focuses on classifying the main types and characteristics of mtDNA variations, analyzes the controversies and limitations of current studies, and outlines future research directions, thereby providing an important reference for exploring the etiology of migraine.