Abstract
Zinc is an essential mineral that is required for normal skeletal growth and bone homeostasis. Furthermore, zinc appears to be able to promote bone regeneration. However, the cellular and molecular pathways through which zinc promotes bone growth, homeostasis, and regeneration are poorly understood. Zinc can positively affect chondrocyte and osteoblast functions, while inhibiting osteoclast activity, consistent with a beneficial role for zinc in bone homeostasis and regeneration. Based on the effects of zinc on skeletal cell populations and the role of zinc in skeletal growth, therapeutic approaches using zinc to improve bone regeneration are being developed. This review focuses on the role of zinc in bone growth, homeostasis, and regeneration while providing an overview of the existing studies that use zinc as a bone regeneration therapeutic.
Highlights
Zinc appears to be able to promote bone regeneration
Zinc transporter ZIP4 and ion channel TRPM7 appear to be critical for zinc absorption in the intestine
Mutations in ZIP4 (Slc39a4) are associated with acrodermatitis enteropathica, a genetic disorder that manifests at weaning and is lethal unless treated by dietary zinc supplementation, indicating that ZIP4 is necessary for intestinal zinc absorption [10,11,12,13,14,15]
Summary
Zinc is an essential mineral required for several cellular processes in the body. In a typical 70 kg human, zinc is the sixth most abundant metal (2.3 g) behind calcium (1 kg), potassium (140 g), sodium (100 g), magnesium (19 g), and iron (4.2 g) and is more abundant than rubidium (0.68 g), strontium (0.32 g), and other trace metals [1]. Targeted deletion of Trpm in the intestine of mice causes post-natal lethality by day 10 with decreased levels of zinc and calcium in serum and bone [17]. Responds to increased intracellular zinc levels by localizing in the nucleus where this transcription factor binds to target genes to affect transcription [20,21,22,23,24]. Zinc appears to promote insulin-related and IGF-1 related signaling by affecting protein tyrosine phosphatase activity [43,44,45]. Grp is a G-protein coupled receptor that responds to extracellular zinc levels to regulate pancreatic β-cell insulin secretion and promotes gastro-intestinal function and integrity [46,47,48]. The following summarizes our current understanding of zinc effects on different bone cell types and experiments showing that zinc can be used to promote bone formation and regeneration
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