Diabetic nephropathy is a leading cause of end-stage renal disease worldwide. The multipronged drug approach targeting blood\r\npressure and serum levels of glucose, insulin, and lipids fails to fully prevent the onset and progression of diabetic nephropathy.\r\nTherefore, a new therapeutic target to combat diabetic nephropathy is required. Autophagy is a catabolic process that degrades\r\ndamaged proteins and organelles in mammalian cells and plays a critical role in maintaining cellular homeostasis.Theaccumulation\r\nof proteins and organelles damaged by hyperglycemia and other diabetes-related metabolic changes is highly associated with the\r\ndevelopment of diabetic nephropathy. Recent studies have suggested that autophagy activity is altered in both podocytes and\r\nproximal tubular cells under diabetic conditions. Autophagy activity is regulated by both nutrient state and intracellular stresses.\r\nUnder diabetic conditions, an altered nutritional state due to nutrient excess may interfere with the autophagic response stimulated\r\nby intracellular stresses, leading to exacerbation of organelle dysfunction and diabetic nephropathy. In this review, we discuss new\r\nfindings showing the relationships between autophagy and diabetic nephropathy and suggest the therapeutic potential of autophagy\r\nin diabetic nephropathy.
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