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10.1681/ASN.2013070798 http://scihub22266oqcxt.onion/10.1681/ASN.2013070798 C3968506!3968506!24262794     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2014 ; 25 (4): 687-92 Nephropedia Template TP {{tp|p=24262794|t=2014. Feasibility of Repairing Glomerular Basement Membrane Defects in Alport Syndrome |pdf=|usr=}}{{24262794}} gab.com Text Feasibility of Repairing Glomerular Basement Membrane Defects in Alport Syndrome JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=24262794 #FOAvip Alport syndrome is a hereditary glomerular disease that leads to kidney failure. It is caused by mutations affecting one of three chains of the collagen ?3?4?5(IV) heterotrimer, which forms the major collagen IV network of the glomerular basement membrane (GBM). In the absence of the ?3?4?5(IV) network, the ?1?1?2(IV) network substitutes, but it is insufficient to maintain normal kidney function. Inhibition of angiotensin-converting enzyme slows progression to kidney failure in patients with Alport syndrome but is not a cure. Restoration of the normal collagen ?3?4?5(IV) network in the GBM, by either cell- or gene-based therapy, is an attractive and logical approach toward a cure, but whether or not the abnormal GBM can be repaired once it has formed and is functioning is unknown. Using a mouse model of Alport syndrome and an inducible transgene system, we found that secretion of ?3?4?5(IV) heterotrimers by podocytes into a preformed, abnormal, filtering Alport GBM is effective at restoring the missing collagen IV network, slowing kidney disease progression, and extending life span. This proof-of-principle study demonstrates the plasticity of the mature GBM and validates the pursuit of therapeutic approaches aimed at normalizing the GBM to prolong kidney function. Twit Text FOAVip Feasibility of Repairing Glomerular Basement Membrane Defects in Alport Syndrome ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=24262794 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24262794 #FOAvip English Wikipedia <ref>{{Cite pmid|24262794}}</ref> Feasibility of Repairing Glomerular Basement Membrane Defects in Alport Syndrome #MMPMID24262794 Lin X; Suh JH; Go G; Miner JH J Am Soc Nephrol 2014[Apr]; 25 (4): 687-92 PMID24262794show ga Alport syndrome is a hereditary glomerular disease that leads to kidney failure. It is caused by mutations affecting one of three chains of the collagen ?3?4?5(IV) heterotrimer, which forms the major collagen IV network of the glomerular basement membrane (GBM). In the absence of the ?3?4?5(IV) network, the ?1?1?2(IV) network substitutes, but it is insufficient to maintain normal kidney function. Inhibition of angiotensin-converting enzyme slows progression to kidney failure in patients with Alport syndrome but is not a cure. Restoration of the normal collagen ?3?4?5(IV) network in the GBM, by either cell- or gene-based therapy, is an attractive and logical approach toward a cure, but whether or not the abnormal GBM can be repaired once it has formed and is functioning is unknown. Using a mouse model of Alport syndrome and an inducible transgene system, we found that secretion of ?3?4?5(IV) heterotrimers by podocytes into a preformed, abnormal, filtering Alport GBM is effective at restoring the missing collagen IV network, slowing kidney disease progression, and extending life span. This proof-of-principle study demonstrates the plasticity of the mature GBM and validates the pursuit of therapeutic approaches aimed at normalizing the GBM to prolong kidney function. äFeasibility of Repairing Glomerular Basement Membrane Defects in Alpor(epmc).pdf DeepDyve Pubget Overpricing