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10.1080/15548627.2015.1049799 http://scihub22266oqcxt.onion/10.1080/15548627.2015.1049799 26039325!4590611!26039325     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Autophagy 2015 ; 11 (7): 1130-45 Nephropedia Template TP {{tp|p=26039325|t=2015. Endothelial cell and podocyte autophagy synergistically protect from diabetes-induced glomerulosclerosis |pdf=|usr=}}{{26039325}} gab.com Text Endothelial cell and podocyte autophagy synergistically protect from diabetes-induced glomerulosclerosis JO: Autophagy http://www.kidney.de/pget.php?&tw=1&pmid=26039325 #FOAvip The glomerulus is a highly specialized capillary tuft, which under pressure filters large amounts of water and small solutes into the urinary space, while retaining albumin and large proteins. The glomerular filtration barrier (GFB) is a highly specialized filtration interface between blood and urine that is highly permeable to small and midsized solutes in plasma but relatively impermeable to macromolecules such as albumin. The integrity of the GFB is maintained by molecular interplay between its 3 layers: the glomerular endothelium, the glomerular basement membrane and podocytes, which are highly specialized postmitotic pericytes forming the outer part of the GFB. Abnormalities of glomerular ultrafiltration lead to the loss of proteins in urine and progressive renal insufficiency, underlining the importance of the GFB. Indeed, albuminuria is strongly predictive of the course of chronic nephropathies especially that of diabetic nephropathy (DN), a leading cause of renal insufficiency. We found that high glucose concentrations promote autophagy flux in podocyte cultures and that the abundance of LC3B II in podocytes is high in diabetic mice. Deletion of Atg5 specifically in podocytes resulted in accelerated diabetes-induced podocytopathy with a leaky GFB and glomerulosclerosis. Strikingly, genetic alteration of autophagy on the other side of the GFB involving the endothelial-specific deletion of Atg5 also resulted in capillary rarefaction and accelerated DN. Thus autophagy is a key protective mechanism on both cellular layers of the GFB suggesting autophagy as a promising new therapeutic strategy for DN. Twit Text FOAVip Endothelial cell and podocyte autophagy synergistically protect from diabetes-induced glomerulosclerosis ????Autophagy http://www.kidney.de/pget.php?&tw=1&pmid=26039325 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26039325 #FOAvip English Wikipedia <ref>{{Cite pmid|26039325}}</ref> Endothelial cell and podocyte autophagy synergistically protect from diabetes-induced glomerulosclerosis #MMPMID26039325 Lenoir O; Jasiek M; Henique C; Guyonnet L; Hartleben B; Bork T; Chipont A; Flosseau K; Bensaada I; Schmitt A; Masse JM; Souyri M; Huber TB; Tharaux PL Autophagy 2015[]; 11 (7): 1130-45 PMID26039325show ga The glomerulus is a highly specialized capillary tuft, which under pressure filters large amounts of water and small solutes into the urinary space, while retaining albumin and large proteins. The glomerular filtration barrier (GFB) is a highly specialized filtration interface between blood and urine that is highly permeable to small and midsized solutes in plasma but relatively impermeable to macromolecules such as albumin. The integrity of the GFB is maintained by molecular interplay between its 3 layers: the glomerular endothelium, the glomerular basement membrane and podocytes, which are highly specialized postmitotic pericytes forming the outer part of the GFB. Abnormalities of glomerular ultrafiltration lead to the loss of proteins in urine and progressive renal insufficiency, underlining the importance of the GFB. Indeed, albuminuria is strongly predictive of the course of chronic nephropathies especially that of diabetic nephropathy (DN), a leading cause of renal insufficiency. We found that high glucose concentrations promote autophagy flux in podocyte cultures and that the abundance of LC3B II in podocytes is high in diabetic mice. Deletion of Atg5 specifically in podocytes resulted in accelerated diabetes-induced podocytopathy with a leaky GFB and glomerulosclerosis. Strikingly, genetic alteration of autophagy on the other side of the GFB involving the endothelial-specific deletion of Atg5 also resulted in capillary rarefaction and accelerated DN. Thus autophagy is a key protective mechanism on both cellular layers of the GFB suggesting autophagy as a promising new therapeutic strategy for DN. |*Autophagy/drug effects[MESH] |Animals[MESH] |Apoptosis/drug effects[MESH] |Autophagy-Related Protein 5[MESH] |Cells, Cultured[MESH] |Diabetic Nephropathies/*pathology/physiopathology/*prevention & control[MESH] |Endothelial Cells/drug effects/*pathology/ultrastructure[MESH] |Gene Deletion[MESH] |Glomerular Filtration Rate/drug effects[MESH] |Glucose/pharmacology[MESH] |Integrases/metabolism[MESH] |Mesangial Cells/drug effects/pathology/ultrastructure[MESH] |Mice, Inbred C57BL[MESH] |Microtubule-Associated Proteins/deficiency/metabolism[MESH] |Phenotype[MESH]Endothelial cell and podocyte autophagy synergistically protect from (epmc).pdf DeepDyve Pubget Overpricing