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本文引用的文献

1
Wnt signaling as a therapeutic target for bone diseases.Wnt信号通路作为骨疾病的治疗靶点
Expert Opin Ther Targets. 2009 Apr;13(4):485-96. doi: 10.1517/14728220902841961.
2
Secreted frizzled related protein 1 is a target to improve fracture healing.分泌型卷曲相关蛋白1是改善骨折愈合的一个靶点。
J Cell Physiol. 2009 Jul;220(1):174-81. doi: 10.1002/jcp.21747.
3
Modulation of Wnt signaling through inhibition of secreted frizzled-related protein I (sFRP-1) with N-substituted piperidinyl diphenylsulfonyl sulfonamides.通过用N-取代哌啶基二苯磺酰基磺酰胺抑制分泌型卷曲相关蛋白1(sFRP-1)来调节Wnt信号通路。
J Med Chem. 2009 Jan 8;52(1):105-16. doi: 10.1021/jm801144h.
4
Sclerostin antibody treatment increases bone formation, bone mass, and bone strength in a rat model of postmenopausal osteoporosis.硬化蛋白抗体治疗可增加绝经后骨质疏松大鼠模型的骨形成、骨量和骨强度。
J Bone Miner Res. 2009 Apr;24(4):578-88. doi: 10.1359/jbmr.081206.
5
Longitudinal in vivo analysis of the region-specific efficacy of parathyroid hormone in a rat cortical defect model.甲状旁腺激素在大鼠皮质缺损模型中区域特异性疗效的纵向体内分析。
Endocrinology. 2009 Apr;150(4):1570-9. doi: 10.1210/en.2008-0814. Epub 2008 Nov 20.
6
Inhibiting Dickkopf-1 (Dkk1) removes suppression of bone formation and prevents the development of osteolytic bone disease in multiple myeloma.抑制Dickkopf-1(Dkk1)可消除对骨形成的抑制,并预防多发性骨髓瘤中溶骨性骨病的发展。
J Bone Miner Res. 2009 Mar;24(3):425-36. doi: 10.1359/jbmr.081104.
7
Parathyroid hormone signaling through low-density lipoprotein-related protein 6.甲状旁腺激素通过低密度脂蛋白相关蛋白6进行信号传导。
Genes Dev. 2008 Nov 1;22(21):2968-79. doi: 10.1101/gad.1702708.
8
Alternative wnt signaling is initiated by distinct receptors.替代性Wnt信号传导由不同的受体启动。
Sci Signal. 2008 Sep 2;1(35):re9. doi: 10.1126/scisignal.135re9.
9
Control of bone mass and remodeling by PTH receptor signaling in osteocytes.骨细胞中甲状旁腺激素受体信号传导对骨量和重塑的调控
PLoS One. 2008 Aug 13;3(8):e2942. doi: 10.1371/journal.pone.0002942.
10
Wnt/beta-catenin signaling: new (and old) players and new insights.Wnt/β-连环蛋白信号传导:新(及旧)参与者与新见解
Curr Opin Cell Biol. 2008 Apr;20(2):119-25. doi: 10.1016/j.ceb.2008.01.009. Epub 2008 Mar 12.

骨折修复过程中的Wnt信号传导。

Wnt signaling during fracture repair.

作者信息

Secreto Frank J, Hoeppner Luke H, Westendorf Jennifer J

机构信息

Departments of Orthopedic Surgery and Biochemistry & Molecular Biology, Mayo Clinic, Rochester, MN 55905, USA.

出版信息

Curr Osteoporos Rep. 2009 Jul;7(2):64-9. doi: 10.1007/s11914-009-0012-5.

DOI:10.1007/s11914-009-0012-5
PMID:19631031
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2972700/
Abstract

Bone is one of the few tissues in the body with the capacity to regenerate and repair itself. Fractures usually are completely repaired in a relatively short time, but in a small percentage of cases, healing never occurs and nonunion is the result. Fracture repair and bone regeneration require the localized reactivation of signaling cascades that are crucial for skeletal development. The Wnt/beta-catenin signaling pathway is one such developmental pathway whose role in bone formation and regeneration recently has been appreciated. During the past decade, much has been learned about how Wnt pathways regulate bone mass. Small molecules and biologics aimed at this pathway are now being tested as potential new anabolic agents. This article reviews recent data demonstrating that Wnt pathways are active during fracture repair and that increasing the activities of Wnt pathway components accelerates bone regeneration.

摘要

骨骼是人体中少数具有自我再生和修复能力的组织之一。骨折通常在相对较短的时间内完全愈合,但在少数情况下,愈合过程无法发生,最终导致骨不连。骨折修复和骨再生需要局部重新激活对骨骼发育至关重要的信号级联反应。Wnt/β-连环蛋白信号通路就是这样一种发育途径,其在骨形成和再生中的作用最近才受到关注。在过去十年中,人们对Wnt通路如何调节骨量有了很多了解。针对该通路的小分子和生物制剂目前正在作为潜在的新型促合成代谢药物进行测试。本文综述了近期数据,这些数据表明Wnt通路在骨折修复过程中是活跃的,并且增加Wnt通路成分的活性可加速骨再生。