【摘要】 糖尿病周围神经病变(diabetic peripheral neuropathy, DPN)是糖尿病最常见的慢性并发症，其中痛性糖尿病周围神经病变(painful diabetic peripheral neuropathy, PDPN)导致的慢性疼痛严重影响病人的生活质量。线粒体作为神经元的主要能量来源，对维持神经元的结构和功能至关重要。大量的研究表明，线粒体与DPN的发病密切相关，其病理机制涉及氧化应激、钙稳态失衡以及能量生成障碍等方面，诱发神经元凋亡，从而引起神经损伤，最终导致神经病理性疼痛。目前许多药物通过调控线粒体功能，发挥镇痛作用，表明调控线粒体功能障碍可能是有效治疗神经病理性疼痛的策略之一。本文将从线粒体功能障碍出发，对其在DPN中的发病机制进行综述，为预防和治疗DPN提供理论参考。更多还原

【Abstract】 Diabetic peripheral neuropathy(DPN) 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.更多还原