Department of Diabetology and Endocrinology, Kanazawa Medical University, Uchinada, Ishikawa, 920-0293, Japan,
Clin Exp Nephrol. 2014 Apr;18(2):210-3. doi: 10.1007/s10157-013-0908-3. Epub 2013 Nov 14.
Autophagy has evolved as a stress response that allows unicellular eukaryotic organisms to survive in starved conditions by regulating energy homeostasis and/or by protein and organelle quality control. The diabetes-induced accumulation of damaged proteins and organelles results in the development and progression of diabetic nephropathy. In contrast, autophagy machinery is activated by calorie restriction and environmental stress in proximal tubular cells, and is maintained at a high level in podocytes, suggesting its crucial role in the pathogenesis of diabetic nephropathy. However, its role in diabetic nephropathy has not been fully known. Here, we will discuss the role of autophagy and its involvement in the pathogenesis of diabetic nephropathy.
自噬作为一种应激反应而进化，通过调节能量稳态和/或通过蛋白质和细胞器质量控制，使单细胞真核生物能够在饥饿条件下存活。糖尿病引起的损伤蛋白和细胞器的积累导致糖尿病肾病的发生和发展。相比之下，自噬机制在近端肾小管细胞中被卡路里限制和环境应激激活，并在足细胞中维持在高水平，表明其在糖尿病肾病发病机制中的关键作用。然而，其在糖尿病肾病中的作用尚未完全清楚。在这里，我们将讨论自噬的作用及其在糖尿病肾病发病机制中的作用。
