PDF(Pubmed)
Abstract：
Muscular dystrophy is a heterogenous group of hereditary muscle disorders caused by mutations in the genes responsible for muscle development, and is generally defined by a disastrous progression of muscle wasting and massive loss in muscle regeneration. Pax7 is closely associated with myogenesis, which is governed by various signaling pathways throughout a lifetime and is frequently used as an indicator in muscle research. In this review, an extensive literature search adhering to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines was performed to identify research that examined signaling pathways in living models, while quantifying Pax7 expression in myogenesis. A total of 247 articles were retrieved from the Web of Science (WoS), PubMed and Scopus databases and were thoroughly examined and evaluated, resulting in 19 articles which met the inclusion criteria. Admittedly, we were only able to discuss the quantification of Pax7 carried out in research affecting various type of genes and signaling pathways, rather than the expression of Pax7 itself, due to the massive differences in approach, factor molecules and signaling pathways analyzed across the research. However, we highlighted the thorough evidence for the alteration of the muscle stem cell precursor Pax7 in multiple signaling pathways described in different living models, with an emphasis on the novel approach that could be taken in manipulating Pax7 expression itself in dystrophic muscle, towards the discovery of an effective treatment for muscular dystrophy. Therefore, we believe that this could be applied to the potential gap in muscle research that could be filled by tuning the well-established marker expression to improve dystrophic muscle.
摘要：
肌营养不良是一组异质性的遗传性肌肉疾病，由负责肌肉发育的基因突变引起，通常定义为肌肉萎缩和肌肉再生大量丧失的灾难性进展。Pax7与肌生成密切相关,它在一生中受到各种信号通路的控制，经常被用作肌肉研究的指标。在这次审查中,根据系统审查和荟萃分析（PRISMA）指南的首选报告项目进行了广泛的文献检索，以确定检查生命模型中信号通路的研究。同时定量Pax7在肌生成中的表达。总共从WebofScience(WoS)检索到247篇文章，PubMed和Scopus数据库，并进行了彻底检查和评估，导致19篇文章符合纳入标准。诚然，我们只能讨论在影响各种类型基因和信号通路的研究中进行的Pax7的定量，而不是Pax7本身的表达，由于方法上的巨大差异，在整个研究中分析了因子分子和信号通路。然而,我们强调了肌肉干细胞前体Pax7在不同生命模型中描述的多种信号通路中改变的全面证据，强调可以在营养不良肌肉中操纵Pax7表达本身的新方法，发现一种有效的治疗肌肉萎缩症的方法。因此,我们认为这可以应用于肌肉研究中的潜在空白,可以通过调整已建立的标记表达来改善营养不良性肌肉来填补这一空白.
