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10.1172/JCI39492 http://scihub22266oqcxt.onion/10.1172/JCI39492 20200449!2846040!20200449     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 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       J+Clin+Invest 2010 ; 120 (4): 1084-96 Nephropedia Template TP {{tp|p=20200449|t=2010. Autophagy influences glomerular disease susceptibility and maintains podocyte homeostasis in aging mice |pdf=|usr=}}{{20200449}} gab.com Text Autophagy influences glomerular disease susceptibility and maintains podocyte homeostasis in aging mice JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=20200449 #FOAvip Injury and loss of podocytes are leading factors of glomerular disease and renal failure. The postmitotic podocyte is the primary glomerular target for toxic, immune, metabolic, and oxidant stress, but little is known about how this cell type copes with stress. Recently, autophagy has been identified as a major pathway that delivers damaged proteins and organelles to lysosomes in order to maintain cellular homeostasis. Here we report that podocytes exhibit an unusually high level of constitutive autophagy. Podocyte-specific deletion of autophagy-related 5 (Atg5) led to a glomerulopathy in aging mice that was accompanied by an accumulation of oxidized and ubiquitinated proteins, ER stress, and proteinuria. These changes resulted ultimately in podocyte loss and late-onset glomerulosclerosis. Analysis of pathophysiological conditions indicated that autophagy was substantially increased in glomeruli from mice with induced proteinuria and in glomeruli from patients with acquired proteinuric diseases. Further, mice lacking Atg5 in podocytes exhibited strongly increased susceptibility to models of glomerular disease. These findings highlight the importance of induced autophagy as a key homeostatic mechanism to maintain podocyte integrity. We postulate that constitutive and induced autophagy is a major protective mechanism against podocyte aging and glomerular injury, representing a putative target to ameliorate human glomerular disease and aging-related loss of renal function. Twit Text FOAVip Autophagy influences glomerular disease susceptibility and maintains podocyte homeostasis in aging mice ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=20200449 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20200449 #FOAvip English Wikipedia <ref>{{Cite pmid|20200449}}</ref> Autophagy influences glomerular disease susceptibility and maintains podocyte homeostasis in aging mice #MMPMID20200449 Hartleben B; Godel M; Meyer-Schwesinger C; Liu S; Ulrich T; Kobler S; Wiech T; Grahammer F; Arnold SJ; Lindenmeyer MT; Cohen CD; Pavenstadt H; Kerjaschki D; Mizushima N; Shaw AS; Walz G; Huber TB J Clin Invest 2010[Apr]; 120 (4): 1084-96 PMID20200449show ga Injury and loss of podocytes are leading factors of glomerular disease and renal failure. The postmitotic podocyte is the primary glomerular target for toxic, immune, metabolic, and oxidant stress, but little is known about how this cell type copes with stress. Recently, autophagy has been identified as a major pathway that delivers damaged proteins and organelles to lysosomes in order to maintain cellular homeostasis. Here we report that podocytes exhibit an unusually high level of constitutive autophagy. Podocyte-specific deletion of autophagy-related 5 (Atg5) led to a glomerulopathy in aging mice that was accompanied by an accumulation of oxidized and ubiquitinated proteins, ER stress, and proteinuria. These changes resulted ultimately in podocyte loss and late-onset glomerulosclerosis. Analysis of pathophysiological conditions indicated that autophagy was substantially increased in glomeruli from mice with induced proteinuria and in glomeruli from patients with acquired proteinuric diseases. Further, mice lacking Atg5 in podocytes exhibited strongly increased susceptibility to models of glomerular disease. These findings highlight the importance of induced autophagy as a key homeostatic mechanism to maintain podocyte integrity. We postulate that constitutive and induced autophagy is a major protective mechanism against podocyte aging and glomerular injury, representing a putative target to ameliorate human glomerular disease and aging-related loss of renal function. |*Autophagy[MESH] |Aging/*physiology[MESH] |Animals[MESH] |Autophagy-Related Protein 5[MESH] |Cells, Cultured[MESH] |Disease Susceptibility[MESH] |Homeostasis[MESH] |Humans[MESH] |Kidney Diseases/*etiology[MESH] |Kidney Glomerulus/*pathology[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Microtubule-Associated Proteins/physiology[MESH] |Podocytes/*physiology[MESH] |Proteasome Endopeptidase Complex/physiology[MESH] |Proteinuria/etiology[MESH] |Stress, Physiological[MESH]Autophagy influences glomerular disease susceptibility and maintains p(epmc).pdf DeepDyve Pubget Overpricing