Akademik Veri Yönetim Sistemi
LIFE-BASEL, cilt.15, sa.8, 2025 (SCI-Expanded)
Migraine is a complex neurological disorder characterized by recurrent headaches and sensory disturbances. Emerging evidence highlights a critical role for mitochondrial dysfunction in migraine pathophysiology, including impairments in oxidative phosphorylation, disruptions in mitochondrial dynamics, and altered biogenesis. Experimental migraine models-ranging from nitroglycerin-induced attacks to inflammatory stimuli-consistently demonstrate mitochondrial swelling, cristae disruption, decreased ATP production, and increased oxidative stress. These findings are accompanied by the altered expression of key mitochondrial regulators such as PGC-1 alpha, Drp1, and Mfn1. Recent studies have further identified distinct metabolic subtypes of mitochondria, including P5CS-containing subsets, which exhibit unique structural and functional profiles, including cristae loss and reduced ATP synthase expression. Notably, the mitochondrial alterations observed in migraine models show remarkable parallels to those described in P5CS-related mitochondrial subsets. These similarities suggest a potential mechanistic link between metabolic reprogramming within mitochondria and migraine pathogenesis. Understanding the contribution of these newly defined mitochondrial populations could offer novel insights into migraine biology and open new avenues for targeted therapeutic strategies.