Interventions against nutrient-sensing pathways represent an emerging new therapeutic approach for diabetic nephropathy.
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.
Department of Diabetology and Endocrinology, Kanazawa Medical University, Uchinada, Ishikawa, 920-0293, Japan, koya0516@kanazawa-med.ac.jp.
Daisuke
D
Koya
Munehiro
M
Kitada
Shinji
S
Kume
Keizo
K
Kanasaki
D000263:Adenylate Kinase / Q000378:metabolism; D000818:Animals; D001343:Autophagy / Q000502:physiology; D003928:Diabetic Nephropathies / Q000188:drug therapy / Q000209:etiology*; D050199:Podocytes / Q000378:metabolism; D037761:Sirtuins / Q000378:metabolism
D000263:Adenylate Kinase; D037761:Sirtuins