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10.1053/j.ackd.2019.08.014 http://scihub22266oqcxt.onion/10.1053/j.ackd.2019.08.014 31831120!ä!31831120 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=31831120&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 219.6 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\31831120.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Adv+Chronic+Kidney+Dis 2019 ; 26 (6): 417-426 Nephropedia Template TP {{tp|p=31831120|t=2019. Mechanisms of Vascular Calcification in Kidney Disease |pdf=|usr=}}{{31831120}} gab.com Text Mechanisms of Vascular Calcification in Kidney Disease JO: Adv Chronic Kidney Dis http://www.kidney.de/pget.php?&tw=1&pmid=31831120 #FOAvip The increase in prevalence and severity of vascular calcification in chronic kidney disease is a result of complex interactions between changes in the vascular bed, mineral metabolites, and other uremic factors. Vascular calcification can occur in the intima and the media of arterial wall. Under permissive conditions, vascular smooth muscle cells (VSMCs) can transform to osteoblast-like phenotype. The membrane-bound vesicles released from transformed VSMCs and the apoptotic bodies derived from dying VSMCs serve as nucleating structures for calcium crystal formation. Alterations in the quality and the quantity of endogenous calcification inhibitors also give rise to an environment that potentiates calcification. Twit Text FOAVip Mechanisms of Vascular Calcification in Kidney Disease ????Adv Chronic Kidney Dis http://www.kidney.de/pget.php?&tw=1&pmid=31831120 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31831120 #FOAvip English Wikipedia <ref>{{Cite pmid|31831120}}</ref> Mechanisms of Vascular Calcification in Kidney Disease #MMPMID31831120 Disthabanchong S; Srisuwarn P Adv Chronic Kidney Dis 2019[Nov]; 26 (6): 417-426 PMID31831120show ga The increase in prevalence and severity of vascular calcification in chronic kidney disease is a result of complex interactions between changes in the vascular bed, mineral metabolites, and other uremic factors. Vascular calcification can occur in the intima and the media of arterial wall. Under permissive conditions, vascular smooth muscle cells (VSMCs) can transform to osteoblast-like phenotype. The membrane-bound vesicles released from transformed VSMCs and the apoptotic bodies derived from dying VSMCs serve as nucleating structures for calcium crystal formation. Alterations in the quality and the quantity of endogenous calcification inhibitors also give rise to an environment that potentiates calcification. |Animals[MESH] |Atherosclerosis/etiology/*metabolism[MESH] |Calcium-Binding Proteins/metabolism[MESH] |Cell Transdifferentiation[MESH] |Endothelium/physiopathology[MESH] |Extracellular Matrix Proteins/metabolism[MESH] |Humans[MESH] |Magnesium/metabolism[MESH] |Matrix Gla Protein[MESH] |Myocytes, Smooth Muscle/*physiology[MESH] |Renal Insufficiency, Chronic/complications/*metabolism[MESH] |Tunica Intima/pathology[MESH] |Vascular Calcification/etiology/*metabolism[MESH]Mechanisms of Vascular Calcification in Kidney Disease (epmc).pdf DeepDyve Pubget Overpricing