Neuropathic pain is a chronic pain condition caused by damage to the nervous system. Its pathogenesis is complex, and effective treatments are limited, significantly impairing patients' quality of life. Mitochondria are the energy supply centers of cells and play a crucial role in maintaining neuronal homeostasis. Growing evidence suggests mitochondrial dysfunction is a key contributor to pain initiation and persistence. However, the role of mitochondrial dysfunction in neuropathic pain has been relatively less studied, and its underlying mechanisms remain unclear. This article reviews the latest research progress on the mechanisms by which mitochondrial dysfunction affects neuropathic pain, with a focus on key pathways including mitochondrial morphological alterations, bioenergetic abnormalities (such as reduced adenosine triphosphate production and decreased membrane potential), dynamic impairments (e.g., disrupted axonal transport, mitochondrial fragmentation, and calcium homeostasis imbalance), enhanced oxidative stress, and impaired mitochondrial autophagy. These mechanisms collectively contribute to neuronal dysfunction and abnormal transmission of pain signals. Additionally, this article elaborates on various therapeutic strategies targeting mitochondrial dysfunction, offering novel insights and scientific evidence for the precise treatment of neuropathic pain.