PDF(Pubmed)
Abstract：
UNASSIGNED: The interaction between muscle and bone is shown to be clinically important but the underlying mechanisms are largely unknown. The canonical Wnt/β-catenin signaling pathway is reported to be involved in muscle-bone crosstalk, but its detailed function remains unclear. This systematic review aims to investigate and elucidate the role of the Wnt/β-catenin signaling pathways in muscle-bone crosstalk.
UNASSIGNED: We conducted a literature search on the Web of Science, PubMed, EBSCO and Embase with keywords \"Wnt*\", \"bone*\" and \"muscle*\". A systematic review was completed according to the guideline of preferred reporting items of systematic reviews and meta-analyses (PRISMA). Data synthesis included species (human, animal or cell type used), treatments involved, outcome measures and key findings with respect to Wnts.
UNASSIGNED: Seventeen papers were published from 2007 to 2021 and were extracted from a total of 1529 search results in the databases of Web of Science (468 papers), PubMed (457 papers), EBSCO (371) and Embase (233). 12 Wnt family members were investigated in the papers, including Wnt1, Wnt2, Wnt2b, Wnt3a, Wnt4, Wnt5a, Wnt8a, Wnt8b, Wnt9a, Wnt10a, Wnt10b and Wnt16. Many studies showed that muscles were able to increase or decrease osteogenesis of bone, while bone increased myogenesis of muscle through Wnt/β-catenin signaling pathways. Wnt3a, Wnt4 and Wnt10b were shown to play important roles in the crosstalk between muscle and bone.
UNASSIGNED: Wnt3a, Wnt4 and Wnt10b are found to play important mediatory roles in muscle-bone crosstalk. The role of Wnt4 was mostly found to regulate muscle from the bone side. Whilst the role of Wnt10b during muscle ageing was proposed, current evidence is insufficient to clarify the specific role of Wnt/β-catenin signaling in the interplay between sarcopenia and osteoporosis. More future studies are required to investigate the exact regulatory roles of Wnts in muscle-bone crosstalk in musculoskeletal disease models such as sarcopenia and osteoporosis.
UNASSIGNED: The systematic review provides an extensive overview to reveal the roles of Wnt/β-catenin signaling pathways in muscle-bone crosstalk. These results provide novel research directions to further understand the underlying mechanism of sarcopenia, osteoporosis, and their crosstalk, finally helping the future development of new therapeutic interventions.
UNASSIGNED: We conducted a literature search on the Web of Science, PubMed, EBSCO and Embase with keywords \"Wnt*\", \"bone*\" and \"muscle*\". A systematic review was completed according to the guideline of preferred reporting items of systematic reviews and meta-analyses (PRISMA). Data synthesis included species (human, animal or cell type used), treatments involved, outcome measures and key findings with respect to Wnts.
UNASSIGNED: Seventeen papers were published from 2007 to 2021 and were extracted from a total of 1529 search results in the databases of Web of Science (468 papers), PubMed (457 papers), EBSCO (371) and Embase (233). 12 Wnt family members were investigated in the papers, including Wnt1, Wnt2, Wnt2b, Wnt3a, Wnt4, Wnt5a, Wnt8a, Wnt8b, Wnt9a, Wnt10a, Wnt10b and Wnt16. Many studies showed that muscles were able to increase or decrease osteogenesis of bone, while bone increased myogenesis of muscle through Wnt/β-catenin signaling pathways. Wnt3a, Wnt4 and Wnt10b were shown to play important roles in the crosstalk between muscle and bone.
UNASSIGNED: Wnt3a, Wnt4 and Wnt10b are found to play important mediatory roles in muscle-bone crosstalk. The role of Wnt4 was mostly found to regulate muscle from the bone side. Whilst the role of Wnt10b during muscle ageing was proposed, current evidence is insufficient to clarify the specific role of Wnt/β-catenin signaling in the interplay between sarcopenia and osteoporosis. More future studies are required to investigate the exact regulatory roles of Wnts in muscle-bone crosstalk in musculoskeletal disease models such as sarcopenia and osteoporosis.
UNASSIGNED: The systematic review provides an extensive overview to reveal the roles of Wnt/β-catenin signaling pathways in muscle-bone crosstalk. These results provide novel research directions to further understand the underlying mechanism of sarcopenia, osteoporosis, and their crosstalk, finally helping the future development of new therapeutic interventions.
摘要：
■显示肌肉和骨骼之间的相互作用在临床上很重要，但潜在的机制在很大程度上是未知的。据报道，经典的Wnt/β-catenin信号通路参与肌肉-骨骼串扰，但其详细功能仍不清楚。本系统综述旨在研究和阐明Wnt/β-catenin信号通路在肌肉-骨骼串扰中的作用。
■我们在WebofScience上进行了文献检索，PubMed,EBSCO和Embase，关键字为“Wnt*”，“骨*”和“肌肉*”。根据系统评价和荟萃分析（PRISMA）的首选报告项目指南完成了系统评价。数据综合包括物种(人类，使用的动物或细胞类型)，涉及的治疗，关于Wnts的结果测量和关键发现。
■从2007年到2021年发表了17篇论文，这些论文是从WebofScience数据库中总共1529个搜索结果中提取的（468篇论文），PubMed(457篇论文)，EBSCO（371）和Embase（233）。在论文中调查了12名Wnt家庭成员，包括Wnt1、Wnt2、Wnt2b、WNT3a,Wnt4,Wnt5a,WNT8a,Wnt8b,Wnt9a,Wnt10a,WNT10b和WNT16。许多研究表明，肌肉能够增加或减少骨骼的成骨，而骨骼通过Wnt/β-catenin信号通路增加肌肉的肌生成。WNT3a,Wnt4和Wnt10b被证明在肌肉和骨骼之间的串扰中起重要作用。
■Wnt3a,发现Wnt4和Wnt10b在肌肉-骨骼串扰中起重要的中介作用。Wnt4的作用主要被发现从骨骼侧调节肌肉。虽然提出了Wnt10b在肌肉老化过程中的作用，目前的证据不足以阐明Wnt/β-catenin信号在少肌症和骨质疏松症之间的相互作用中的具体作用。需要更多的未来研究来研究Wnts在肌肉骨骼疾病模型（如肌肉减少症和骨质疏松症）中肌肉-骨骼串扰中的确切调节作用。
■系统综述提供了广泛的概述，以揭示Wnt/β-catenin信号通路在肌肉-骨骼串扰中的作用。这些结果为进一步理解肌肉减少症的潜在机制提供了新的研究方向。骨质疏松,和他们的相声，最后帮助未来开发新的治疗干预措施。
■我们在WebofScience上进行了文献检索，PubMed,EBSCO和Embase，关键字为“Wnt*”，“骨*”和“肌肉*”。根据系统评价和荟萃分析（PRISMA）的首选报告项目指南完成了系统评价。数据综合包括物种(人类，使用的动物或细胞类型)，涉及的治疗，关于Wnts的结果测量和关键发现。
■从2007年到2021年发表了17篇论文，这些论文是从WebofScience数据库中总共1529个搜索结果中提取的（468篇论文），PubMed(457篇论文)，EBSCO（371）和Embase（233）。在论文中调查了12名Wnt家庭成员，包括Wnt1、Wnt2、Wnt2b、WNT3a,Wnt4,Wnt5a,WNT8a,Wnt8b,Wnt9a,Wnt10a,WNT10b和WNT16。许多研究表明，肌肉能够增加或减少骨骼的成骨，而骨骼通过Wnt/β-catenin信号通路增加肌肉的肌生成。WNT3a,Wnt4和Wnt10b被证明在肌肉和骨骼之间的串扰中起重要作用。
■Wnt3a,发现Wnt4和Wnt10b在肌肉-骨骼串扰中起重要的中介作用。Wnt4的作用主要被发现从骨骼侧调节肌肉。虽然提出了Wnt10b在肌肉老化过程中的作用，目前的证据不足以阐明Wnt/β-catenin信号在少肌症和骨质疏松症之间的相互作用中的具体作用。需要更多的未来研究来研究Wnts在肌肉骨骼疾病模型（如肌肉减少症和骨质疏松症）中肌肉-骨骼串扰中的确切调节作用。
■系统综述提供了广泛的概述，以揭示Wnt/β-catenin信号通路在肌肉-骨骼串扰中的作用。这些结果为进一步理解肌肉减少症的潜在机制提供了新的研究方向。骨质疏松,和他们的相声，最后帮助未来开发新的治疗干预措施。
