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These reactive aldehydes further disrupt mitochondrial function, activate pro-inflammatory pathways (e.g., NF-B), and sensitize nociceptive neurons, contributing to neuroinflammation, neuronal dysfunction in FM ( Mitochondrial dysfunction in FM is evident from reduced electron transport chain (ETC) activity, lower oxygen consumption in muscle biopsies, and diminished bioenergetic reserve ( Neuronal and microglial mitochondrial dysfunction in FM impairs electron transport chain (ETC) activity, leading to electron leakage and superoxide (O ) formation, which contribute to ATP deficits