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10.1172/jci.insight.95091 http://scihub22266oqcxt.onion/10.1172/jci.insight.95091 C5916242!5916242 !29467330     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29467330 &cmd=llinks): Failed to open stream: HTTP request failed! 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Inducible podocyte-specific deletion of CTCF drives progressive kidney disease and bone abnormalities |pdf=|usr=}}{{29467330 }} gab.com Text Inducible podocyte-specific deletion of CTCF drives progressive kidney disease and bone abnormalities JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=29467330 #FOAvip Progressive chronic kidney diseases (CKDs) are on the rise worldwide. However, the sequence of events resulting in CKD progression remain poorly understood. Animal models of CKD exploring these issues are confounded by systemic toxicities or surgical interventions to acutely induce kidney injury. Here we report the generation of a CKD mouse model through the inducible podocyte-specific ablation of an essential endogenous molecule, the chromatin structure regulator CCCTC-binding factor (CTCF), which leads to rapid podocyte loss (iCTCFpod-/-). As a consequence, iCTCFpod-/- mice develop severe progressive albuminuria, hyperlipidemia, hypoalbuminemia, and impairment of renal function, and die within 8-10 weeks. CKD progression in iCTCFpod-/- mice leads to high serum phosphate and elevations in fibroblast growth factor 23 (FGF23) and parathyroid hormone that rapidly cause bone mineralization defects, increased bone resorption, and bone loss. Dissection of the timeline leading to glomerular pathology in this CKD model led to the surprising observation that podocyte ablation and the resulting glomerular filter destruction is sufficient to drive progressive CKD and osteodystrophy in the absence of interstitial fibrosis. This work introduces an animal model with significant advantages for the study of CKD progression, and it highlights the need for podocyte-protective strategies for future kidney therapeutics. Twit Text FOAVip Inducible podocyte-specific deletion of CTCF drives progressive kidney disease and bone abnormalities ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=29467330 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29467330 #FOAvip English Wikipedia <ref>{{Cite pmid|29467330 }}</ref> Inducible podocyte-specific deletion of CTCF drives progressive kidney disease and bone abnormalities #MMPMID29467330 Christov M ; Clark AR ; Corbin B ; Hakroush S ; Rhee EP ; Saito H ; Brooks D ; Hesse E ; Bouxsein M ; Galjart N ; Jung JY ; Mundel P ; Jüppner H ; Weins A ; Greka A JCI Insight 2018[Feb]; 3 (4 ): ä PMID29467330 show ga Progressive chronic kidney diseases (CKDs) are on the rise worldwide. However, the sequence of events resulting in CKD progression remain poorly understood. Animal models of CKD exploring these issues are confounded by systemic toxicities or surgical interventions to acutely induce kidney injury. Here we report the generation of a CKD mouse model through the inducible podocyte-specific ablation of an essential endogenous molecule, the chromatin structure regulator CCCTC-binding factor (CTCF), which leads to rapid podocyte loss (iCTCFpod-/-). As a consequence, iCTCFpod-/- mice develop severe progressive albuminuria, hyperlipidemia, hypoalbuminemia, and impairment of renal function, and die within 8-10 weeks. CKD progression in iCTCFpod-/- mice leads to high serum phosphate and elevations in fibroblast growth factor 23 (FGF23) and parathyroid hormone that rapidly cause bone mineralization defects, increased bone resorption, and bone loss. Dissection of the timeline leading to glomerular pathology in this CKD model led to the surprising observation that podocyte ablation and the resulting glomerular filter destruction is sufficient to drive progressive CKD and osteodystrophy in the absence of interstitial fibrosis. This work introduces an animal model with significant advantages for the study of CKD progression, and it highlights the need for podocyte-protective strategies for future kidney therapeutics. |*Disease Models, Animal [MESH] |Animals [MESH] |Bone Resorption/blood/*etiology/pathology [MESH] |CCCTC-Binding Factor/*deficiency/genetics [MESH] |Calcification, Physiologic/genetics [MESH] |Disease Progression [MESH] |Female [MESH] |Fibroblast Growth Factor-23 [MESH] |Fibroblast Growth Factors/blood [MESH] |Glomerular Filtration Rate [MESH] |Humans [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Parathyroid Hormone/blood [MESH] |Podocytes/*pathology [MESH]Inducible podocyte-specific deletion of CTCF drives progressive kidney(epmc).pdf DeepDyve Pubget Overpricing