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10.1681/ASN.2013111202 http://scihub22266oqcxt.onion/10.1681/ASN.2013111202 25406339!4413752!25406339     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25406339.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Am+Soc+Nephrol 2015 ; 26 (5): 1040-52 Nephropedia Template TP {{tp|p=25406339|t=2015. Deficient Autophagy Results in Mitochondrial Dysfunction and FSGS |pdf=|usr=}}{{25406339}} gab.com Text Deficient Autophagy Results in Mitochondrial Dysfunction and FSGS JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25406339 #FOAvip FSGS is a heterogeneous fibrosing disease of the kidney, the cause of which remains poorly understood. In most cases, there is no effective treatment to halt or retard progression to renal failure. Increasing evidence points to mitochondrial dysfunction and the generation of reactive oxygen species in the pathogenesis of CKD. Autophagy, a major intracellular lysosomal degradation system, performs homeostatic functions linked to metabolism and organelle turnover. We prevented normal autophagic pathways in nephrons of mice by mutating critical autophagy genes ATG5 or ATG7 during nephrogenesis. Mutant mice developed mild podocyte and tubular dysfunction within 2 months, profound glomerular and tubular changes bearing close similarity to human disease by 4 months, and organ failure by 6 months. Ultrastructurally, podocytes and tubular cells showed vacuolization, abnormal mitochondria, and evidence of endoplasmic reticulum stress, features that precede the appearance of histologic or clinical disease. Similar changes were observed in human idiopathic FSGS kidney biopsy specimens. Biochemical analysis of podocytes and tubules of 2-month-old mutant mice revealed elevated production of reactive oxygen species, activation of endoplasmic reticulum stress pathways, phosphorylation of p38, and mitochondrial dysfunction. Furthermore, cultured proximal tubule cells isolated from mutant mice showed marked mitochondrial dysfunction and elevated mitochondrial reactive oxygen species generation that was suppressed by a mitochondrial superoxide scavenger. We conclude that mitochondrial dysfunction and endoplasmic reticulum stress due to impaired autophagic organelle turnover in podocytes and tubular epithelium are sufficient to cause many of the manifestations of FSGS in mice. Twit Text FOAVip Deficient Autophagy Results in Mitochondrial Dysfunction and FSGS ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25406339 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25406339 #FOAvip English Wikipedia <ref>{{Cite pmid|25406339}}</ref> Deficient Autophagy Results in Mitochondrial Dysfunction and FSGS #MMPMID25406339 Kawakami T; Gomez IG; Ren S; Hudkins K; Roach A; Alpers CE; Shankland SJ; D'Agati VD; Duffield JS J Am Soc Nephrol 2015[May]; 26 (5): 1040-52 PMID25406339show ga FSGS is a heterogeneous fibrosing disease of the kidney, the cause of which remains poorly understood. In most cases, there is no effective treatment to halt or retard progression to renal failure. Increasing evidence points to mitochondrial dysfunction and the generation of reactive oxygen species in the pathogenesis of CKD. Autophagy, a major intracellular lysosomal degradation system, performs homeostatic functions linked to metabolism and organelle turnover. We prevented normal autophagic pathways in nephrons of mice by mutating critical autophagy genes ATG5 or ATG7 during nephrogenesis. Mutant mice developed mild podocyte and tubular dysfunction within 2 months, profound glomerular and tubular changes bearing close similarity to human disease by 4 months, and organ failure by 6 months. Ultrastructurally, podocytes and tubular cells showed vacuolization, abnormal mitochondria, and evidence of endoplasmic reticulum stress, features that precede the appearance of histologic or clinical disease. Similar changes were observed in human idiopathic FSGS kidney biopsy specimens. Biochemical analysis of podocytes and tubules of 2-month-old mutant mice revealed elevated production of reactive oxygen species, activation of endoplasmic reticulum stress pathways, phosphorylation of p38, and mitochondrial dysfunction. Furthermore, cultured proximal tubule cells isolated from mutant mice showed marked mitochondrial dysfunction and elevated mitochondrial reactive oxygen species generation that was suppressed by a mitochondrial superoxide scavenger. We conclude that mitochondrial dysfunction and endoplasmic reticulum stress due to impaired autophagic organelle turnover in podocytes and tubular epithelium are sufficient to cause many of the manifestations of FSGS in mice. |Animals[MESH] |Autophagy[MESH] |Autophagy-Related Protein 5[MESH] |Autophagy-Related Protein 7[MESH] |Disease Models, Animal[MESH] |Endoplasmic Reticulum Stress[MESH] |Glomerulosclerosis, Focal Segmental/*etiology/metabolism/pathology[MESH] |Humans[MESH] |Mice[MESH] |Microtubule-Associated Proteins/*deficiency/genetics[MESH] |Mitochondria/*physiology/ultrastructure[MESH] |Mutation[MESH] |Podocytes/*physiology[MESH] |Reactive Oxygen Species/metabolism[MESH] |Retrospective Studies[MESH]Deficient Autophagy Results in Mitochondrial Dysfunction and FSGS (epmc).pdf DeepDyve Pubget Overpricing