VDR Activation Reduces Proteinuria and High-Glucose-Induced Injury of Kidneys and Podocytes by Regulating Wnt Signaling Pathway
Author(s) -
Jia Guo,
Congqun Lu,
Fangxing Zhang,
Haixia Yu,
Mengwen Zhou,
Meixia He,
Chunyan Wang,
Zhanzheng Zhao,
Zhangsuo Liu
Publication year - 2017
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000480315
Subject(s) - calcitriol receptor , wnt signaling pathway , paricalcitol , endocrinology , diabetic nephropathy , proteinuria , medicine , sclerostin , podocyte , kidney , agonist , signal transduction , receptor , vitamin d and neurology , parathyroid hormone , biology , microbiology and biotechnology , secondary hyperparathyroidism , calcium
Diabetic nephropathy (DN) is a major cause of end-stage renal disease and proteinuria is one of the most prominent clinical manifestations. The expression of Vitamin D receptor (VDR) in patients with chronic kidney diseases was decreased, while VDR agonists could partially alleviate the proteinuria of DN in animal models. The present study was designed to determine the expression of VDR in renal tissues and its relationship with proteinuria the diabetic model db/db mice.
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