Redox reactions in chronic pain: mechanisms and relevance in fibromyalgia.

Fibromyalgia (FM) is increasingly recognized as a disorder driven by oxidative stress, mitochondrial dysfunction, and neuroinflammation, contributing to pain sensitization and fatigue. This review explores the role of redox imbalance in FM and evaluates potential therapeutic interventions. A scoping literature search was conducted using PubMed, Scopus, and Google Scholar. Findings indicate elevated oxidative stress markers (MDA, 4-HNE), impaired antioxidant defenses [CoQ10 (Coenzyme Q10), SOD, catalase], and mitochondrial dysfunction in FM patients. Preclinical and small-scale clinical studies suggest potential benefits of NRF2 activation, high-dose thiamine, CoQ10, molecular hydrogen, and oxygen-ozone (O₂O₃) therapy. However, human trial evidence is limited, and standardized treatment protocols are lacking. Given the absence of robust RCTs, oxidative stress modulation in FM remains investigational. Future research should prioritize high-quality RCTs to establish the efficacy, safety, and clinical application of redox-targeted therapies.