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NR Restores Mitochondrial Function and Reduces Trigeminal Pain: Preclinical Findings
Synopsis
In a mouse model of trigeminal neuropathic pain, the injured trigeminal ganglion (TG) showed profound mitochondrial dysfunction, affecting gene expression, protein synthesis, and respiratory activity. Increasing NAD+ levels with nicotinamide riboside (NR) markedly improved mitochondrial health and significantly reduced craniofacial pain behaviors. The analgesic effect depended largely on Sirt1, and multi-omics analyses showed that NR-activated Sirt1 suppressed a wide array of pain-related and inflammatory genes in the TG. These results demonstrate that mitochondrial impairment is a key driver of trigeminal neuropathic pain and that restoring mitochondrial function—particularly through NAD+–Sirt1 activation—represents a promising therapeutic strategy for severe craniofacial pain such as trigeminal neuralgia.
Journal
Free Radical Biology and Medicine