Vitamin D in Vascular Calcification: A Double-Edged Sword?
Vascular calcification (VC) as a manifestation of perturbed mineral balance, is associated with aging, diabetes and kidney dysfunction, as well as poorer patient outcomes. Due to the current limited understanding of the pathophysiology of vascular calcification, the development of effective preventa...
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doaj-4c8fe48a8bf94a2facc20acd38a94d572020-11-25T00:38:56ZengMDPI AGNutrients2072-66432018-05-0110565210.3390/nu10050652nu10050652Vitamin D in Vascular Calcification: A Double-Edged Sword?Jeffrey Wang0Jimmy J. Zhou1Graham R. Robertson2Vincent W. Lee3Centre for Transplantation and Renal Research, Westmead Institute of Medical Research, Westmead, NSW 2145, AustraliaCentre for Transplantation and Renal Research, Westmead Institute of Medical Research, Westmead, NSW 2145, AustraliaCellmid Limited, 2/55 Clarence St, Sydney, NSW 2000, AustraliaCentre for Transplantation and Renal Research, Westmead Institute of Medical Research, Westmead, NSW 2145, AustraliaVascular calcification (VC) as a manifestation of perturbed mineral balance, is associated with aging, diabetes and kidney dysfunction, as well as poorer patient outcomes. Due to the current limited understanding of the pathophysiology of vascular calcification, the development of effective preventative and therapeutic strategies remains a significant clinical challenge. Recent evidence suggests that traditional risk factors for cardiovascular disease, such as left ventricular hypertrophy and dyslipidaemia, fail to account for clinical observations of vascular calcification. Therefore, more complex underlying processes involving physiochemical changes to mineral balance, vascular remodelling and perturbed hormonal responses such as parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF-23) are likely to contribute to VC. In particular, VC resulting from modifications to calcium, phosphate and vitamin D homeostasis has been recently elucidated. Notably, deregulation of vitamin D metabolism, dietary calcium intake and renal mineral handling are associated with imbalances in systemic calcium and phosphate levels and endothelial cell dysfunction, which can modulate both bone and soft tissue calcification. This review addresses the current understanding of VC pathophysiology, with a focus on the pathogenic role of vitamin D that has provided new insights into the mechanisms of VC.http://www.mdpi.com/2072-6643/10/5/652vascular calcificationosteogenic differentiationcalciumphosphatevitamin Dhypervitaminosishypovitaminosisbiphasic |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Jeffrey Wang Jimmy J. Zhou Graham R. Robertson Vincent W. Lee |
spellingShingle |
Jeffrey Wang Jimmy J. Zhou Graham R. Robertson Vincent W. Lee Vitamin D in Vascular Calcification: A Double-Edged Sword? Nutrients vascular calcification osteogenic differentiation calcium phosphate vitamin D hypervitaminosis hypovitaminosis biphasic |
author_facet |
Jeffrey Wang Jimmy J. Zhou Graham R. Robertson Vincent W. Lee |
author_sort |
Jeffrey Wang |
title |
Vitamin D in Vascular Calcification: A Double-Edged Sword? |
title_short |
Vitamin D in Vascular Calcification: A Double-Edged Sword? |
title_full |
Vitamin D in Vascular Calcification: A Double-Edged Sword? |
title_fullStr |
Vitamin D in Vascular Calcification: A Double-Edged Sword? |
title_full_unstemmed |
Vitamin D in Vascular Calcification: A Double-Edged Sword? |
title_sort |
vitamin d in vascular calcification: a double-edged sword? |
publisher |
MDPI AG |
series |
Nutrients |
issn |
2072-6643 |
publishDate |
2018-05-01 |
description |
Vascular calcification (VC) as a manifestation of perturbed mineral balance, is associated with aging, diabetes and kidney dysfunction, as well as poorer patient outcomes. Due to the current limited understanding of the pathophysiology of vascular calcification, the development of effective preventative and therapeutic strategies remains a significant clinical challenge. Recent evidence suggests that traditional risk factors for cardiovascular disease, such as left ventricular hypertrophy and dyslipidaemia, fail to account for clinical observations of vascular calcification. Therefore, more complex underlying processes involving physiochemical changes to mineral balance, vascular remodelling and perturbed hormonal responses such as parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF-23) are likely to contribute to VC. In particular, VC resulting from modifications to calcium, phosphate and vitamin D homeostasis has been recently elucidated. Notably, deregulation of vitamin D metabolism, dietary calcium intake and renal mineral handling are associated with imbalances in systemic calcium and phosphate levels and endothelial cell dysfunction, which can modulate both bone and soft tissue calcification. This review addresses the current understanding of VC pathophysiology, with a focus on the pathogenic role of vitamin D that has provided new insights into the mechanisms of VC. |
topic |
vascular calcification osteogenic differentiation calcium phosphate vitamin D hypervitaminosis hypovitaminosis biphasic |
url |
http://www.mdpi.com/2072-6643/10/5/652 |
work_keys_str_mv |
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