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10.1016/j.kint.2019.09.034 http://scihub22266oqcxt.onion/10.1016/j.kint.2019.09.034 31866113!ä!31866113 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Kidney+Int 2020 ; 97 (3): 487-501 Nephropedia Template TP {{tp|p=31866113|t=2020. Magnesium prevents vascular calcification in Klotho deficiency |pdf=|usr=}}{{31866113}} gab.com Text Magnesium prevents vascular calcification in Klotho deficiency JO: Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=31866113 #FOAvip Klotho knock-out mice are an important model for vascular calcification, which is associated with chronic kidney disease. In chronic kidney disease, serum magnesium inversely correlates with vascular calcification. Here we determine the effects of serum magnesium on aortic calcification in Klotho knock-out mice treated with a minimal or a high magnesium diet from birth. After eight weeks, serum biochemistry and aorta and bone tissues were studied. Protective effects of magnesium were characterized by RNA-sequencing of the aorta and micro-CT analysis was performed to study bone integrity. A high magnesium diet prevented vascular calcification and aortic gene expression of Runx2 and matrix Gla protein found in such mice on the minimal magnesium diet. Differential expression of inflammation and extracellular matrix remodeling genes accompanied the beneficial effects of magnesium on calcification. High dietary magnesium did not affect serum parathyroid hormone, 1,25-dihydroxyvitamin D(3) or calcium. High magnesium intake prevented vascular calcification despite increased fibroblast growth factor-23 and phosphate concentration in the knock-out mice. Compared to mice on the minimal magnesium diet, the high magnesium diet reduced femoral bone mineral density by 20% and caused excessive osteoid formation indicating osteomalacia. Osteoclast activity was unaffected by the high magnesium diet. In Saos-2 osteoblasts, magnesium supplementation reduced mineralization independent of osteoblast function. Thus, high dietary magnesium prevents calcification in Klotho knock-out mice. These effects are potentially mediated by reduction of inflammatory and extracellular matrix remodeling pathways within the aorta. Hence magnesium treatment may be promising to prevent vascular calcification, but the risk for osteomalacia should be considered. Twit Text FOAVip Magnesium prevents vascular calcification in Klotho deficiency ????Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=31866113 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31866113 #FOAvip English Wikipedia <ref>{{Cite pmid|31866113}}</ref> Magnesium prevents vascular calcification in Klotho deficiency #MMPMID31866113 Ter Braake AD; Smit AE; Bos C; van Herwaarden AE; Alkema W; van Essen HW; Bravenboer N; Vervloet MG; Hoenderop JGJ; de Baaij JHF Kidney Int 2020[Mar]; 97 (3): 487-501 PMID31866113show ga Klotho knock-out mice are an important model for vascular calcification, which is associated with chronic kidney disease. In chronic kidney disease, serum magnesium inversely correlates with vascular calcification. Here we determine the effects of serum magnesium on aortic calcification in Klotho knock-out mice treated with a minimal or a high magnesium diet from birth. After eight weeks, serum biochemistry and aorta and bone tissues were studied. Protective effects of magnesium were characterized by RNA-sequencing of the aorta and micro-CT analysis was performed to study bone integrity. A high magnesium diet prevented vascular calcification and aortic gene expression of Runx2 and matrix Gla protein found in such mice on the minimal magnesium diet. Differential expression of inflammation and extracellular matrix remodeling genes accompanied the beneficial effects of magnesium on calcification. High dietary magnesium did not affect serum parathyroid hormone, 1,25-dihydroxyvitamin D(3) or calcium. High magnesium intake prevented vascular calcification despite increased fibroblast growth factor-23 and phosphate concentration in the knock-out mice. Compared to mice on the minimal magnesium diet, the high magnesium diet reduced femoral bone mineral density by 20% and caused excessive osteoid formation indicating osteomalacia. Osteoclast activity was unaffected by the high magnesium diet. In Saos-2 osteoblasts, magnesium supplementation reduced mineralization independent of osteoblast function. Thus, high dietary magnesium prevents calcification in Klotho knock-out mice. These effects are potentially mediated by reduction of inflammatory and extracellular matrix remodeling pathways within the aorta. Hence magnesium treatment may be promising to prevent vascular calcification, but the risk for osteomalacia should be considered. |*Renal Insufficiency, Chronic[MESH] |*Vascular Calcification/genetics/prevention & control[MESH] |Animals[MESH] |Glucuronidase/*deficiency/genetics[MESH] |Klotho Proteins[MESH] |Magnesium/*pharmacology[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Parathyroid Hormone[MESH]Magnesium prevents vascular calcification in Klotho deficiency (epmc).pdf DeepDyve Pubget Overpricing