Diabetic nephropathy (DN) is a chronic complication of diabetes mellitus (DM) with approximately 30–40% of patients with DM developing nephropathy, and it is the leading cause of end-stage renal diseases and diabetic morbidity. The pathogenesis of DN is primarily associated with irregularities in the metabolism of glucose and lipid leading to hyperglycemia-induced oxidative stress, which has been a major target together with blood pressure regulation in the control of DN progression. However, the regulation of 5′ adenosine monophosphate-activated protein kinase (AMPK), a highly conserved protein kinase for maintaining energy balance and cellular growth and repair has been implicated in the development of DM and its complications. Therefore, targeting AMPK pathway has been explored as a therapeutic strategy for the treatment of diabetes and its complication, although most of the mechanisms have not been fully elucidated. In this review, we discuss the structure of AMPK relevant to understanding its allosteric regulation and its role in the pathogenesis and progression of DN. We also identify therapeutic agents that modulate AMPK and its downstream targets with their specific mechanisms of action in the treatment of DN.

糖尿病肾病（DN）是糖尿病（DM）的慢性并发症，约30–40％的DM患者发展为肾病，它是终末期肾脏疾病和糖尿病发病率的主要原因。DN的发病机理主要与导致高血糖症引起的氧化应激的葡萄糖和脂质代谢异常有关，这已成为控制DN进展的主要目标以及血压调节。然而，5'腺苷单磷酸激活蛋白激酶（AMPK）是一种高度保守的蛋白激酶，用于维持能量平衡以及细胞生长和修复，其调控与糖尿病及其并发症的发生有关。因此，尽管大多数机制尚未完全阐明，但靶向AMPK途径的药物已被探索为治疗糖尿病及其并发症的治疗策略。在这篇综述中，我们讨论了与了解AMPK的变构调节及其在DN的发病机理和进展中的作用有关的AMPK的结构。我们还确定了可调节AMPK及其下游靶标的治疗剂，其在DN的治疗中具有特定的作用机制。