Kwon Jae-Hee, Kim Do-Kyun, Cho Young-Eun, Kwun In-Sook
Department of Food and Nutrition, College of Life Science and Biotechnology, Andong National University, Andong 36729, Korea.
Korea Zoonosis Research Institute, Jeonbuk National University, Iksan 54531, Korea.
Prev Nutr Food Sci. 2024 Jun 30;29(2):118-124. doi: 10.3746/pnf.2024.29.2.118.
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.
尽管锌在骨钙化中的作用已得到充分证实，但其在血管钙化中的作用仍不明确。血管钙化的特征是软组织中钙和磷异常沉积，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。本综述重点关注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，锌缺乏会诱导VSMC和主动脉钙化，主要是通过细胞凋亡伴随平滑肌细胞标志物的下调。此外，锌缺乏诱导的血管钙化独立于通常与成骨过程相关的碱性磷酸酶（ALP）活性起作用，但部分通过无机磷酸盐转运体-1（Pit-1）调节。迄今为止，研究表明锌通过一种不同于成骨钙化的机制调节血管钙化，这为其对生理和病理钙化的双重作用提供了见解，从而解释了“锌悖论”，即锌同时增加成骨细胞钙化并减少VSMC钙化。
