Restoring the Physiology of Vitamin D Receptor Activation and the Concept of Selectivity

2011 ◽  
pp. 151-156 ◽  
Author(s):  
Mario Cozzolino ◽  
Irene Brenna ◽  
Elisa Volpi ◽  
Paola Ciceri ◽  
Florjan Mehmeti ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Receptor Activation

Vitamin D receptor activation raises soluble thrombomodulin levels in chronic kidney disease patients: a double blind, randomized trial

2018 ◽  
Vol 34 (5) ◽  
pp. 819-824 ◽  
Author(s):  
Graziella D’arrigo ◽  
Patrizia Pizzini ◽  
Sebastiano Cutrupi ◽  
Rocco Tripepi ◽  
Giovanni Tripepi ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Randomized Trial ◽  
Vitamin D Receptor ◽  
Receptor Activation ◽  
Double Blind ◽  
Soluble Thrombomodulin

Structural Insights into the Molecular Mechanism of Vitamin D Receptor Activation by Lithocholic Acid Involving a New Mode of Ligand Recognition

2014 ◽  
Vol 57 (11) ◽  
pp. 4710-4719 ◽  
Author(s):  
Anna Y. Belorusova ◽  
Jérôme Eberhardt ◽  
Noëlle Potier ◽  
Roland H. Stote ◽  
Annick Dejaegere ◽  
...  
Keyword(s):  
Vitamin D ◽  
Molecular Mechanism ◽  
Vitamin D Receptor ◽  
Lithocholic Acid ◽  
Receptor Activation ◽  
Ligand Recognition ◽  
Structural Insights

scholarly journals SP322ADIPONECTIN MODIFIES THE FGF23 RESPONSE TO VITAMIN D RECEPTOR ACTIVATION: A RANDOMIZED CLINICAL TRIAL

2018 ◽  
Vol 33 (suppl_1) ◽  
pp. i452-i452
Author(s):  
Belinda Spoto ◽  
Patrizia Pizzini ◽  
Giovanni Tripepi ◽  
Francesca Mallamaci ◽  
Carmine Zoccali
Keyword(s):  
Clinical Trial ◽  
Vitamin D ◽  
Randomized Clinical Trial ◽  
Vitamin D Receptor ◽  
Receptor Activation

scholarly journals VITAMIN D RECEPTOR ACTIVATION AND A NOVEL CLASSIFICATION OF CARDIO-RENAL SYNDROME

2012 ◽  
Vol 31 (2) ◽  
pp. A27
Author(s):  
Sirous Darabian ◽  
Manoch Rattanasompattikul ◽  
Parta Hatamizadeh ◽  
Suphamai Bunnapradist ◽  
Matthew J. Budoff ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Receptor Activation

Reprint of: Vitamin D receptor activation and prevention of arterial ageing

2013 ◽  
Vol 23 ◽  
pp. S31-S36 ◽  
Author(s):  
M. Cozzolino ◽  
A. Stucchi ◽  
M.A. Rizzo ◽  
L. Soldati ◽  
D. Cusi ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Receptor Activation

scholarly journals The Therapeutic Effect of Active Vitamin D Supplementation in Preventing the Progression of Diabetic Nephropathy in a Diabetic Mouse Model

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Nakhoul Nakhoul ◽  
Tina Thawko ◽  
Evgeny Farber ◽  
Inbal Dahan ◽  
Hagar Tadmor ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Vitamin D ◽  
Diabetic Nephropathy ◽  
Vitamin D Receptor ◽  
Receptor Activation ◽  
Receptor Expression ◽  
Active Vitamin ◽  
Active Vitamin D ◽  
Vitamin D Analog

Background. Diabetic nephropathy (DN) is one of the most common microvascular complications of diabetes and is the leading cause of end-stage renal disease (ESRD) and replacement therapy worldwide. Vitamin D levels in DN patients are very low due to the decrease in the synthesis and activity of 1-α hydroxylase in the proximal tubule cells and decrease in the vitamin D receptor abundance. To date, few studies have shown the antioxidant effects of 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3] on hyperglycemia-induced renal injury. The selective activator of the vitamin D receptor, paricalcitol, reduces proteinuria and slows the progression of kidney injury. The precise mechanism through which vitamin D affects diabetic status and provides kidney protection remains to be determined. Methods. Diabetes mellitus (DM) was induced in 94 8-week-old DBA/2J mice by intraperitoneal injection of streptozotocin (STZ). DM mice were randomly divided into receiving vehicle or treatment with paricalcitol, the active vitamin D analog, 1 week after DM induction or paricalcitol treatment 3 weeks after DM induction. An additional control group of healthy wild-type mice was not treated. Urine albumin, blood urea nitrogen, and creatinine levels were measured before and at the end of the paricalcitol treatment. Periodic acid-Schiff, immunohistochemistry staining, and western blot of the renal tissues of vitamin D receptor, villin, nephrin, and podocin expressions, were analyzed. Results. Paricalcitol treatment restored villin, nephrin, and podocin protein levels that were downregulated upon DM induction, and reduced fibronectin protein level. Vitamin D receptor activation by paricalcitol may reduce proteinuria of DN in mice and alleviate high-glucose-induced injury of kidney podocytes by regulating the key molecules such nephrin-podocin. Conclusions. Paricalcitol treatment was associated with improved structural changes in type 1 diabetic mice including upregulation of vitamin D receptor expression, and decreased fibrosis markers such as fibronectin. These effects may contribute to the consistent benefit of vitamin D analog to slow the deterioration in glomerular function and reduce the risk of ESRD in patients with type 1 and 2 diabetes mellitus. Our results suggest that additional use of paricalcitol may be beneficial in treating patients with diabetes under standard therapeutic strategies.

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