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Autophagic Punctum

Emerging role of podocyte autophagy in the progression of diabetic nephropathy

, , , &
Pages 2385-2386 | Received 19 Oct 2015, Accepted 27 Oct 2015, Published online: 06 Jan 2016

Figures & data

Figure 1. Autophagy insufficiency is associated with the pathogenesis of podocyte injury and massive proteinuria in diabetic nephropathy. Diabetes alone results in the development of mild glomerular lesions, such as glomerular hypertrophy, basement membrane (GBM) thickening, mild mesangial expansion and minimal proteinuria, leading to slowly-progressive renal dysfunction. However, the combination of insufficient podocyte autophagy and diabetic conditions results in podocyte loss, foot process alterations and lysosome dysfunction. This results in massive refractory proteinuria and a rapid decline of renal function. Autophagy insufficiency-related podocyte loss may be involved in the "point of no return" in diabetic nephropathy.

Figure 1. Autophagy insufficiency is associated with the pathogenesis of podocyte injury and massive proteinuria in diabetic nephropathy. Diabetes alone results in the development of mild glomerular lesions, such as glomerular hypertrophy, basement membrane (GBM) thickening, mild mesangial expansion and minimal proteinuria, leading to slowly-progressive renal dysfunction. However, the combination of insufficient podocyte autophagy and diabetic conditions results in podocyte loss, foot process alterations and lysosome dysfunction. This results in massive refractory proteinuria and a rapid decline of renal function. Autophagy insufficiency-related podocyte loss may be involved in the "point of no return" in diabetic nephropathy.

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