Fibroblast Growth Factor-23 Helps Explain the Biphasic Cardiovascular Effects of Vitamin D in Chronic Kidney Disease

<p>Hypovitaminosis D is highly prevalent in chronic kidney disease (CKD). Recently, vitamin D has sparked widespread interest because of its potential favorable benefits on cardiovascular disease (CVD). Evidence from clinical studies and animal models supports the existence of biphasic cardiov...

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Main Author: Peng Hu, Qiang Xuan, Bo Hu, Ling Lu, Jing Wang, Yuan Han Qin
Format: Article
Language:English
Published: Ivyspring International Publisher 2012-01-01
Series:International Journal of Biological Sciences
Online Access:http://www.biolsci.org/v08p0663.htm
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spelling doaj-65e0fdab51e04431930b65e08265d3db2020-11-24T21:30:41ZengIvyspring International PublisherInternational Journal of Biological Sciences1449-22882012-01-0185663671Fibroblast Growth Factor-23 Helps Explain the Biphasic Cardiovascular Effects of Vitamin D in Chronic Kidney DiseasePeng Hu, Qiang Xuan, Bo Hu, Ling Lu, Jing Wang, Yuan Han Qin<p>Hypovitaminosis D is highly prevalent in chronic kidney disease (CKD). Recently, vitamin D has sparked widespread interest because of its potential favorable benefits on cardiovascular disease (CVD). Evidence from clinical studies and animal models supports the existence of biphasic cardiovascular effects of vitamin D, in which lower doses suppress CVD and higher doses stimulate CVD. However, the mechanism for the different effects remains unclear. Fibroblast growth factor-23 (FGF-23) is a recently identified member of the FGF family, and thought to be actively involved in renal phosphate and vitamin D homeostasis. More specifically, Vitamin D stimulates FGF-23 secretion and is inhibited by increased FGF-23. Given this background, we hypothesize that FGF-23 may provide a unique tool to explain the biphasic cardiovascular effects of vitamin D in CKD. The data presented in this review support the hypothesis that FGF-23 may be linked with the high cardiovascular risk in CKD through accelerating the onset of vascular calcification, secondary hyperparathyroidism, left ventricular hypertrophy and endothelial dysfunction. Therefore, modulation of FGF-23 may become a potential therapeutic target to lowing cardiovascular risk in CKD. Several clinical interventions, including decreased phosphate intake, phosphate binders, cinacalcet plus concurrent low-dose vitamin D, C-terminal tail of FGF-23 and renal transplantation, have been employed to manipulate FGF-23.</p>http://www.biolsci.org/v08p0663.htm
collection DOAJ
language English
format Article
sources DOAJ
author Peng Hu, Qiang Xuan, Bo Hu, Ling Lu, Jing Wang, Yuan Han Qin
spellingShingle Peng Hu, Qiang Xuan, Bo Hu, Ling Lu, Jing Wang, Yuan Han Qin
Fibroblast Growth Factor-23 Helps Explain the Biphasic Cardiovascular Effects of Vitamin D in Chronic Kidney Disease
International Journal of Biological Sciences
author_facet Peng Hu, Qiang Xuan, Bo Hu, Ling Lu, Jing Wang, Yuan Han Qin
author_sort Peng Hu, Qiang Xuan, Bo Hu, Ling Lu, Jing Wang, Yuan Han Qin
title Fibroblast Growth Factor-23 Helps Explain the Biphasic Cardiovascular Effects of Vitamin D in Chronic Kidney Disease
title_short Fibroblast Growth Factor-23 Helps Explain the Biphasic Cardiovascular Effects of Vitamin D in Chronic Kidney Disease
title_full Fibroblast Growth Factor-23 Helps Explain the Biphasic Cardiovascular Effects of Vitamin D in Chronic Kidney Disease
title_fullStr Fibroblast Growth Factor-23 Helps Explain the Biphasic Cardiovascular Effects of Vitamin D in Chronic Kidney Disease
title_full_unstemmed Fibroblast Growth Factor-23 Helps Explain the Biphasic Cardiovascular Effects of Vitamin D in Chronic Kidney Disease
title_sort fibroblast growth factor-23 helps explain the biphasic cardiovascular effects of vitamin d in chronic kidney disease
publisher Ivyspring International Publisher
series International Journal of Biological Sciences
issn 1449-2288
publishDate 2012-01-01
description <p>Hypovitaminosis D is highly prevalent in chronic kidney disease (CKD). Recently, vitamin D has sparked widespread interest because of its potential favorable benefits on cardiovascular disease (CVD). Evidence from clinical studies and animal models supports the existence of biphasic cardiovascular effects of vitamin D, in which lower doses suppress CVD and higher doses stimulate CVD. However, the mechanism for the different effects remains unclear. Fibroblast growth factor-23 (FGF-23) is a recently identified member of the FGF family, and thought to be actively involved in renal phosphate and vitamin D homeostasis. More specifically, Vitamin D stimulates FGF-23 secretion and is inhibited by increased FGF-23. Given this background, we hypothesize that FGF-23 may provide a unique tool to explain the biphasic cardiovascular effects of vitamin D in CKD. The data presented in this review support the hypothesis that FGF-23 may be linked with the high cardiovascular risk in CKD through accelerating the onset of vascular calcification, secondary hyperparathyroidism, left ventricular hypertrophy and endothelial dysfunction. Therefore, modulation of FGF-23 may become a potential therapeutic target to lowing cardiovascular risk in CKD. Several clinical interventions, including decreased phosphate intake, phosphate binders, cinacalcet plus concurrent low-dose vitamin D, C-terminal tail of FGF-23 and renal transplantation, have been employed to manipulate FGF-23.</p>
url http://www.biolsci.org/v08p0663.htm
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