Wu Zeng, Gao Yu, Zuo Chun-Yue, Wang Xiao-Rong, Chen Xiao-Han, Zhou Xiao-Hong, Gao Wei-Juan
Hebei Key Laboratory of Chinese Medicine Research on Cardio-Cerebrovascular Disease, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, China.
Diabetol Metab Syndr. 2025 May 14;17(1):154. doi: 10.1186/s13098-025-01718-4.
Diabetic nephropathy (DN) is one of the most common and serious microvascular complications of diabetes mellitus (DM) and is the main cause of end-stage renal disease. Endothelial dysfunction caused by persistent hyperglycemia occurs at the initial stage of vascular disease. Moreover, persistent hyperglycemia is also a critical factor causing renal microcirculatory dysfunction. In recent years, many studies have confirmed that chronic hypoxia caused by microcirculatory dysfunction is one of the main mechanisms of kidney injury in patients with DM. Similarly, microcirculatory dysfunction damages renal tissue through interactions with other pathophysiological processes, thereby promoting the occurrence and development of DN. Thus, this article reviews the pathogenesis of renal microcirculatory dysfunction in DM and its interaction with stress, energy metabolism, and immunologic inflammation. Furthermore, a new idea was proposed to analyze the mechanism of kidney injury in DM from the perspective of microcirculatory dysfunction.
糖尿病肾病（DN）是糖尿病（DM）最常见且最严重的微血管并发症之一，也是终末期肾病的主要病因。持续性高血糖导致的内皮功能障碍发生在血管疾病的初始阶段。此外，持续性高血糖也是导致肾微循环功能障碍的关键因素。近年来，许多研究证实，微循环功能障碍引起的慢性缺氧是糖尿病患者肾损伤的主要机制之一。同样，微循环功能障碍通过与其他病理生理过程相互作用损害肾组织，从而促进DN的发生和发展。因此，本文综述了糖尿病患者肾微循环功能障碍的发病机制及其与应激、能量代谢和免疫炎症的相互作用。此外，还提出了一个新的观点，即从微循环功能障碍的角度分析糖尿病患者肾损伤的机制。
