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Phosphorus overload and PTH induce aortic expression of Runx2 in experimental uraemia
Author(s) -
Fabiana G. Graciolli,
Kátia R. Neves,
Luciene M. dos Reis,
Rafael G. Graciolli,
Irene L. Noronha,
Rosa Maria Affonso Moysés,
Vanda Jorgetti
Publication year - 2008
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfn686
Subject(s) - endocrinology , medicine , parathyroid hormone , runx2 , kidney disease , hyperphosphatemia , osteopontin , osteoprotegerin , phosphate , calcification , parathyroidectomy , downregulation and upregulation , osteoblast , calcium , chemistry , in vitro , biochemistry , receptor , activator (genetics) , gene
Vascular calcification (VC) is commonly seen in patients with chronic kidney disease (CKD). Elevated levels of phosphate and parathormone (PTH) are considered nontraditional risk factors for VC. It has been shown that, in vitro, phosphate transforms vascular smooth muscle cells (VSMCs) into calcifying cells, evidenced by upregulated expression of runt-related transcription factor 2 (Runx2), whereas PTH is protective against VC. In addition, Runx2 has been detected in calcified arteries of CKD patients. However, the in vivo effect of phosphate and PTH on Runx2 expression remains unknown.

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