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首页> 外文期刊>Journal of Cellular Physiology >Role of fibroblast growth factor 2 and wnt signaling in anabolic effects of parathyroid hormone on bone formation
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Role of fibroblast growth factor 2 and wnt signaling in anabolic effects of parathyroid hormone on bone formation

机译：纤维母细胞生长因子2和wnt的角色信号在甲状旁腺合成代谢的影响激素对骨形成

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摘要

Osteoporosis poses enormous health and economic burden worldwide. One of the very few anabolic agents for osteoporosis is parathyroid hormone (PTH). Although great progress has been made since the FDA approved PTH in 2002, the detailed mechanisms of the bone anabolic effects of intermittent PTH treatment is still not well understood. PTH bone anabolic effect is regulated by extracellular factors. Maximal bone anabolic effect of PTH requires fibroblast growth factor 2 (FGF2) signaling, which might be mediated by transcription factor activating transcription factor 4 (ATF4). Maximal bone anabolic effect of PTH also requires Wnt signaling. Particularly, Wnt antagonists such as sclerostin, dickkopf 1 (DKK1) and secreted frizzled related protein 1 (sFRP1) are promising targets to increase bone formation. Interestingly, FGF2 signaling modulates Wnt/β-Catenin signaling pathway in bone. Therefore, multiple signaling pathways utilized by PTH are cross talking and working together to promote bone formation. Extensive studies on the mechanisms of action of PTH will help to identify new pathways that regulate bone formation, to improve available agents to stimulate bone formation, and to identify potential new anabolic agents for osteoporosis.
机译：骨质疏松症带来了巨大的健康和经济全球负担。药物对骨质疏松症是甲状旁腺激素(素。自2002年FDA批准了甲状旁腺素,详细机制的骨合成代谢的影响间歇性甲状旁腺素治疗还没有好理解。由细胞外因素。甲状旁腺素的效果需要纤维母细胞生长因子2(FGF2)信号,这可能是由转录因子激活转录因子4 (ATF4)。甲状旁腺素也需要Wnt信号。Wnt拮抗剂如sclerostin dickkopf 1(DKK1)和分泌卷曲的相关蛋白1增加骨(sFRP1)承诺目标形成。调节Wnt /β连环蛋白信号通路骨头。利用甲状旁腺素是交叉谈话和工作共同促进骨形成。甲状旁腺素的作用机制研究帮助识别调节骨的新途径形成,改善可用的代理刺激骨形成,并识别潜在的新合成药物对骨质疏松症。

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