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Zinc Action in Vascular Calcification.
Kwon, Jae-Hee; Kim, Do-Kyun; Cho, Young-Eun; Kwun, In-Sook.
Afiliação
  • Kwon JH; Department of Food and Nutrition, College of Life Science and Biotechnology, Andong National University, Andong 36729, Korea.
  • Kim DK; Korea Zoonosis Research Institute, Jeonbuk National University, Iksan 54531, Korea.
  • Cho YE; Department of Food and Nutrition, College of Life Science and Biotechnology, Andong National University, Andong 36729, Korea.
  • Kwun IS; Department of Food and Nutrition, College of Life Science and Biotechnology, Andong National University, Andong 36729, Korea.
Prev Nutr Food Sci ; 29(2): 118-124, 2024 Jun 30.
Article em En | MEDLINE | ID: mdl-38974586
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.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article