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

Vitamin D in Vascular Calcification: A Double-Edged Sword?
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DOI:
10.3390/nu10050652
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发表时间:
2018-05-22
期刊:
影响因子:
5.9
通讯作者:
Lee VW
Lee VW
中科院分区:
医学2区
文献类型:
--
作者:
Wang J;Zhou JJ;Robertson GR;Lee VW

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血管钙化(VC)是矿物质平衡紊乱的一种表现,与衰老、糖尿病和肾功能障碍以及较差的患者预后相关。由于目前对血管钙化病理生理学的了解有限,开发有效的预防和治疗策略仍然是一个重大的临床挑战。最近的证据表明,心血管疾病的传统危险因素,如左心室肥厚和血脂异常,无法解释血管钙化的临床观察结果。因此,涉及矿物质平衡的物理化学变化、血管重塑和甲状旁腺激素 (PTH) 和成纤维细胞生长因子 23 (FGF-23) 等激素反应紊乱的更复杂的潜在过程可能会导致 VC。特别是,最近阐明了钙、磷酸盐和维生素 D 稳态改变所产生的 VC。值得注意的是,维生素 D 代谢、膳食钙摄入和肾脏矿物质处理的失调与全身钙和磷酸盐水平失衡以及内皮细胞功能障碍有关,而内皮细胞功能障碍可以调节骨和软组织钙化。这篇综述阐述了目前对 VC 病理生理学的理解,重点关注维生素 D 的致病作用,为 VC 的机制提供了新的见解。
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.
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