Neuropathic pain currently lacks effective individualized therapy regimen. Mitochondria dysfunction is an important mechanism of neuropathic pain. Hyperglycemia, chemotherapy agents and traumas can impair mitochondrial function, cause disordered cellular energy production, abnormal reactive oxygen metabolism, the dysfunction of mitochondrial permeability transition pore, apoptosis, abnormal autophagy and calcium ion uptake and result in the development of neuropathic pain. This article will illuminate the effects and mechanisms of mitochondrial dysfunction on neuropathic pain, and explain the current state and future prospect of mitochondria‑targeted neuropathic pain therapy, so as to provide new thoughts for targeted therapy of neuropathic pain.