Zinc Action in Vascular Calcification.

IF 1.6 Q3 FOOD SCIENCE & TECHNOLOGY
Jae-Hee Kwon, Do-Kyun Kim, Young-Eun Cho, In-Sook Kwun
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引用次数: 0

Abstract

Although zinc's involvement in bone calcification is well-established, its role in vascular calcification, characterized by abnormal calcium and phosphorus deposition in soft tissues and a key aspect of various vascular diseases, including atherosclerosis, remains unclear. This review focuses on zinc's action in vascular smooth muscle cell (VSMC) calcification, including the vascular calcification mechanism. Accumulated research has indicated that zinc deficiency induces calcification in VSMCs and the aorta, primarily through apoptosis accompanied by a downregulation of smooth muscle cell markers. Moreover, zinc deficiency-induced vascular calcification operates independently of the action of alkaline phosphatase (ALP) activity, typically associated with osteogenic processes, but is partly regulated via inorganic phosphate transporter-1 (Pit-1). To date, research has shown that zinc regulates vascular calcification through a mechanism distinct from that of osteogenic calcification, providing insight into its dual effects on physiological and pathological calcification and thereby explaining the "zinc paradox," wherein zinc simultaneously increases osteoblastic calcification and decreases VSMC calcification.

锌在血管钙化中的作用
虽然锌在骨骼钙化中的作用已得到证实,但它在血管钙化中的作用仍不清楚,血管钙化的特点是钙和磷在软组织中的异常沉积,是包括动脉粥样硬化在内的各种血管疾病的一个关键方面。本综述将重点讨论锌在血管平滑肌细胞(VSMC)钙化中的作用,包括血管钙化机制。大量研究表明,缺锌会诱导血管平滑肌细胞(VSMC)和主动脉钙化,主要是通过细胞凋亡和平滑肌细胞标志物的下调。此外,缺锌诱导的血管钙化与碱性磷酸酶(ALP)活性的作用无关,后者通常与成骨过程有关,但部分受无机磷酸盐转运体-1(Pit-1)的调节。迄今为止的研究表明,锌调节血管钙化的机制不同于成骨钙化的机制,这使人们了解了锌对生理性和病理性钙化的双重作用,从而解释了 "锌悖论",即锌同时增加成骨细胞钙化和减少血管内皮细胞钙化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Preventive Nutrition and Food Science
Preventive Nutrition and Food Science Agricultural and Biological Sciences-Food Science
CiteScore
3.40
自引率
0.00%
发文量
35
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