Possible roles of mitochondrial dysfunction in neuropathy.

OBJECTIVES: The present review aims to present and discuss the consistent and inconsistent evidence regarding the associations between mitochondrial dysfunction and several neuropathic models, including trauma-induced, chemotherapy-induced, diabetes-induced and HIV-associated sensory neuropathy. METHODS: The searching strategy and inclusion criteria for this review are all research articles in the PubMed database published before July 2019. We used the search terms 'mitochondria' and 'neuropathy' for the present review and non-English articles were excluded. RESULTS: Damage to mitochondria via trauma, chemotherapy drugs, hyperglycaemia and HIV infection has been widely discussed to play an important role in the pathogenesis of neuropathy. Several mechanisms of mitochondrial damages have been proposed. CONCLUSION: The damage of mitochondria results in cellular apoptosis, which appears to be one of the key factors in the pathogenesis of neuropathy. Novel therapeutic strategies targeting mitochondria could be a potential therapeutic target in neuropathy.

Effect of coenzyme Q10 on mitochondrial respiratory proteins in trigeminal neuralgia.

Trigeminal neuralgia (TN) is the neuropathic pain. Mitochondrial dysfunction, increased oxidative stress, and inflammation demonstrated in chronic pain. Carbamazepine (CBZ) is the first-line drug for TN, however, it is still insufficient. Coenzyme Q10 (CoQ10) has been used as the additional supplement for pain therapy. Nonetheless, mitochondrial respiratory proteins, oxidative stress, and inflammation in TN, and the add-on effects of CoQ10 on those defects have never been investigated. CBZ-treated TN-patients, naïve TN-patients, and control subjects were included. CBZ-treated TN-patients were randomised into two subgroups, received either CoQ10 or placebo for 2 months. Pain levels were evaluated, and peripheral blood mononuclear cells were isolated to determine the oxidative stress, mitochondrial oxidative phosphorylation (OXPHOS), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and cytokines including TNF-α, IL-1ß and IL-18 mRNA expression. Pain scales, oxidative stress, and OXPHOS levels were greater in naïve TN-patients than control, whereas the cytokine profiles were unchanged. Although pain scales were lower in CBZ-treated TN-patients than in naïve TN-patients, oxidative stress, OXPHOS, and cytokine expression profiles were not different. PGC-1α levels found to be increased in CBZ-treated TN patients when compared with the naïve group. CoQ10 supplement in CBZ-treated TN patients reduced pain scale and oxidative stress and increased antioxidants levels when compared with placebo group. However, OXPHOS, PGC-1α, and cytokines were not different between groups. These findings suggest that increased oxidative stress could be potentially involved in the pathogenesis of TN. CoQ10 supplements can reduce oxidative stress, leading to more effective pain reduction in TN patients being treated with CBZ.