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10.1038/nrneph.2013.111 http://scihub22266oqcxt.onion/10.1038/nrneph.2013.111 23774819!ä!23774819 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23774819&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 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\23774819.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Nat+Rev+Nephrol 2013 ; 9 (11): 650-60 Nephropedia Template TP {{tp|p=23774819|t=2013. Klotho, phosphate and FGF-23 in ageing and disturbed mineral metabolism |pdf=|usr=}}{{23774819}} gab.com Text Klotho, phosphate and FGF-23 in ageing and disturbed mineral metabolism JO: Nat Rev Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=23774819 #FOAvip High concentrations of extracellular phosphate are toxic to cells. Impaired urinary phosphate excretion increases serum phosphate level and induces a premature-ageing phenotype. Urinary phosphate levels are increased by dietary phosphate overload and might induce tubular injury and interstitial fibrosis. Extracellular phosphate exerts its cytotoxic effects by forming insoluble nanoparticles with calcium and fetuin-A; these nanoparticles are referred to in this Review as calciprotein particles. Calciprotein particles are highly bioactive ligands that can induce various cellular responses, including the osteogenic transformation of vascular smooth muscle cells and cell death of vascular endothelial cells and renal tubular epithelial cells. Calciprotein particles are detected in the serum of animal models of kidney disease and in patients with chronic kidney disease (CKD) and might be associated with a (mal)adaptation of the endocrine axes mediated by fibroblast growth factors and Klothos that regulate phosphate homeostasis and ageing. These observations raise the possibility that calciprotein particles contribute to the pathogenesis of CKD. This theory, if verified, is expected to provide novel diagnostic markers and therapeutic targets in CKD. Twit Text FOAVip Klotho, phosphate and FGF-23 in ageing and disturbed mineral metabolism ????Nat Rev Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=23774819 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23774819 #FOAvip English Wikipedia <ref>{{Cite pmid|23774819}}</ref> Klotho, phosphate and FGF-23 in ageing and disturbed mineral metabolism #MMPMID23774819 Kuro-o M Nat Rev Nephrol 2013[Nov]; 9 (11): 650-60 PMID23774819show ga High concentrations of extracellular phosphate are toxic to cells. Impaired urinary phosphate excretion increases serum phosphate level and induces a premature-ageing phenotype. Urinary phosphate levels are increased by dietary phosphate overload and might induce tubular injury and interstitial fibrosis. Extracellular phosphate exerts its cytotoxic effects by forming insoluble nanoparticles with calcium and fetuin-A; these nanoparticles are referred to in this Review as calciprotein particles. Calciprotein particles are highly bioactive ligands that can induce various cellular responses, including the osteogenic transformation of vascular smooth muscle cells and cell death of vascular endothelial cells and renal tubular epithelial cells. Calciprotein particles are detected in the serum of animal models of kidney disease and in patients with chronic kidney disease (CKD) and might be associated with a (mal)adaptation of the endocrine axes mediated by fibroblast growth factors and Klothos that regulate phosphate homeostasis and ageing. These observations raise the possibility that calciprotein particles contribute to the pathogenesis of CKD. This theory, if verified, is expected to provide novel diagnostic markers and therapeutic targets in CKD. |Aging/*physiology[MESH] |Animals[MESH] |Fibroblast Growth Factor-23[MESH] |Fibroblast Growth Factors/*physiology[MESH] |Glucuronidase/*physiology[MESH] |Humans[MESH] |Hyperphosphatemia/etiology/metabolism/*physiopathology[MESH] |Klotho Proteins[MESH] |Minerals/metabolism[MESH] |Phosphates/*physiology[MESH]Klotho, phosphate and FGF-23 in ageing and disturbed mineral metabolis(epmc).pdf DeepDyve Pubget Overpricing