Abstract:Diabetic peripheral neuropathy is the most common chronic complication of diabetes, in which chronic pain caused by painful diabetic peripheral neuropathy (pDPN) seriously affects patients" quality of life. As the main energy source of neurons, mitochondria are crucial for maintaining the structure and function of neurons. A large number of studies have shown that mitochondria is closely related to the pathogenesis of pDPN, and its pathological mechanism involves oxidative stress, calcium homeostasis imbalance and energy generation disturbance, which induces neuronal apoptosis, thereby causing nerve damage and ultimately lead to neuropathic pain. At present, many drugs exert analgesic effects by regulating mitochondrial function, suggesting that regulating mitochondrial dysfunction may be the effective strategies to treat neuropathic pain. This article will review the pathogenesis of mitochondrial dysfunction in DPN, hoping to provide theoretical reference for the prevention and treatment of DPN.