Zinc signal: a new player in osteobiology

被引：53

作者：

Fukada, Toshiyuki ^{[1
,2
]}

Hojyo, Shintaro ^{[1
]}

Furuichi, Tatsuya ^{[3
]}

机构：

[1] RIKEN Res Ctr Allergy & Immunol, Lab Cytokine Signaling, Yokohama, Kanagawa 2300045, Japan

[2] Osaka Univ, Grad Sch Med, Dept Allergy & Immunol, Suita, Osaka 5650871, Japan

[3] Iwate Univ, Dept Vet Med Sci, Lab Lab Anim Sci & Med, Fac Agr, Morioka, Iwate 0208550, Japan

来源：

JOURNAL OF BONE AND MINERAL METABOLISM | 2013年 / 31卷 / 02期

关键词：

Zinc; Transporter; Bone; Growth; Signal; ACRODERMATITIS-ENTEROPATHICA; GROWTH-PLATE; DIETARY ZINC; TRANSPORTERS ZIP4; DEFICIENCY; GENE; MOUSE; SLC39A4; PROTEIN; MICE;

D O I：

10.1007/s00774-012-0409-6

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Disturbed zinc (Zn) homeostasis in mammals is mainly characterized by impaired bone generation accompanied with growth retardation. However, the underlying mechanisms that determine how Zn controls bone homeostasis remain to be defined. Zn homeostasis is tightly controlled by Zn transporter families. Recent studies have shown that Zn transporter-mediated Zn ion (Zn2+) behaves as a signaling factor, called Zn signal, that exerts a multiple function in cellular events, showing why Zn has a vital effect on mammalian bone growth and regeneration. This perspective put importance on the principal mechanisms of Zn participation in mammalian bone homeostasis, shifting our focus on the role of Zn from simply a nutrient to a signaling molecule that fine-tunes intracellular signaling events.

引用

页码：129 / 135

页数：7

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