Yasuda-Yamahara Mako, Kume Shinji, Maegawa Hiroshi
Department of Medicine, Shiga University of Medical Science, Tsukinowa-cho, Seta, Otsu, Shiga 520-2192, Japan.
Antioxidants (Basel). 2021 Feb 22;10(2):321. doi: 10.3390/antiox10020321.
Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease and the number of patients affected is increasing worldwide. Thus, there is a need to establish a new treatment for DKD to improve the renal prognosis of diabetic patients. Recently, it has shown that intracellular metabolic abnormalities are involved in the pathogenesis of DKD. In particular, the activity of mechanistic target of rapamycin complex 1 (mTORC1), a nutrient-sensing signaling molecule, is hyperactivated in various organs of diabetic patients, which suggests the involvement of excessive mTORC1 activation in the pathogenesis of diabetes. In DKD, hyperactivated mTORC1 may be involved in the pathogenesis of podocyte damage, which causes proteinuria, and tubular cell injury that decreases renal function. Therefore, elucidating the role of mTORC1 in DKD and developing new therapeutic agents that suppress mTORC1 hyperactivity may shed new light on DKD treatments in the future.
糖尿病肾病（DKD）是终末期肾病的主要病因，全球受影响的患者数量正在增加。因此，需要建立一种新的DKD治疗方法，以改善糖尿病患者的肾脏预后。最近的研究表明，细胞内代谢异常参与了DKD的发病机制。特别是，作为一种营养感应信号分子的雷帕霉素复合物1（mTORC1）机制靶点的活性在糖尿病患者的各个器官中过度激活，这表明mTORC1过度激活参与了糖尿病的发病机制。在DKD中，过度激活的mTORC1可能参与足细胞损伤的发病机制，足细胞损伤会导致蛋白尿，以及肾小管细胞损伤，进而降低肾功能。因此，阐明mTORC1在DKD中的作用，并开发抑制mTORC1过度活性的新型治疗药物，可能为未来DKD的治疗带来新的思路。
