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Nutrients. 2018 May 22;10(5). pii: E652. doi: 10.3390/nu10050652.

Vitamin D in Vascular Calcification: A Double-Edged Sword?

Author information

1
Centre for Transplantation and Renal Research, Westmead Institute of Medical Research, Westmead, NSW 2145, Australia. jwan3534@uni.sydney.edu.au.
2
Centre for Transplantation and Renal Research, Westmead Institute of Medical Research, Westmead, NSW 2145, Australia. jimmy.zhou@health.nsw.gov.au.
3
Centre for Kidney Research, Children's Hospital at Westmead, Westmead, NSW 2145, Australia. jimmy.zhou@health.nsw.gov.au.
4
Cellmid Limited, 2/55 Clarence St, Sydney, NSW 2000, Australia. robertson@cellmid.com.au.
5
Centre for Transplantation and Renal Research, Westmead Institute of Medical Research, Westmead, NSW 2145, Australia. vincent_lee@wmi.usyd.edu.au.

Abstract

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.

KEYWORDS:

biphasic; calcium; hypervitaminosis; hypovitaminosis; osteogenic differentiation; phosphate; vascular calcification; vitamin D

PMID:
29786640
PMCID:
PMC5986531
DOI:
10.3390/nu10050652
[Indexed for MEDLINE]
Free PMC Article

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