慢性肾脏病骨骼肌的分子变化:系统综述

Limy Wong, Rachel Kenny, Jennifer Howard, Lawrence P. McMahon
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摘要

背景 慢性肾脏病(CKD)患者普遍存在骨骼肌质量下降的问题。它与严重的发病率和死亡率有关。其潜在的分子发病机制尚未完全明了。本系统综述旨在总结目前有关 CKD 患者和啮齿类动物骨骼肌分子变化的证据,并评估这些证据的强度。 方法 使用三个主题对 PubMed 和 EMBASE 数据库进行检索:信使核糖核酸/蛋白质/microRNA 表达、骨骼肌和 CKD。本研究按照系统综述和荟萃分析首选报告项目(PRISMA)标准进行。 结果 总共有 98 项研究被纳入系统综述,其中包括 26 项前瞻性人类临床研究、4 项人类和啮齿动物研究以及 68 项纯啮齿动物研究(分别为 32 个小鼠模型和 36 个大鼠模型)。人类研究的样本量大多较小(40% 的研究参与者少于 20 人)。定性聚合酶链反应(qPCR)是最常用的基因表达方法,但没有一项研究符合《qPCR 实验发表最低信息量》的质量评估标准。大多数研究只调查了几个基因或特定的信号通路。FBXO32、TRIM63、MSTN、IL6、TNF 和 IGF1 是调查最多的基因。已确定的差异表达基因和蛋白质属于八种主要通路,包括细胞凋亡、自噬、炎症、胰岛素/胰岛素样生长因子 1 信号传导、脂质代谢、线粒体功能、肌肉细胞生长和分化以及蛋白质降解,这与其他慢性疾病状态类似。 结论 目前有关慢性肾脏病患者骨骼肌分子改变的证据主要来自小型和异质性研究。CKD 和其他慢性疾病的主要生物通路发生了明显的相似变化,这支持了产生肌肉萎缩的共同有害分子机制,而与潜在的特定疾病无关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Molecular changes in skeletal muscle in chronic kidney disease: A systematic review

Background

Loss of skeletal muscle mass is prevalent among patients affected by chronic kidney disease (CKD). It is associated with significant morbidity and mortality. The underlying molecular pathogenesis has yet to be fully understood. The aim of this systematic review is to summarize the current evidence on molecular changes in the skeletal muscle of humans and rodents with CKD and to assess the strength of such evidence.

Methods

The PubMed and EMBASE databases were searched using three main themes: messenger ribonucleic acid/protein/microRNA expression, skeletal muscle and CKD. This study was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) standards.

Results

A total of 98 studies were included in the systematic review, comprising 26 prospective human clinical studies, four human and rodent studies, and 68 rodent-only studies (32 mouse and 36 rat models respectively). The sample sizes of human studies were largely small (40% of studies had ≤20 participants). Qualitative polymerase chain reaction (qPCR) was the most commonly used method for gene expression and none of the studies fulfilled the Minimum Information for Publication of qPCR Experiments criteria for quality assessment. Majority of the studies investigated only a few genes or a specific signalling pathway. FBXO32, TRIM63, MSTN, IL6, TNF and IGF1 were the most investigated genes. The identified differentially expressed genes and proteins belonged to eight major pathways, including apoptosis, autophagy, inflammation, insulin/insulin-like growth factor 1 signalling, lipid metabolism, mitochondrial function, muscle cell growth and differentiation, and protein degradation, similar to other chronic disease states.

Conclusions

The current evidence regarding molecular alterations in the skeletal muscle in CKD is largely derived from small and heterogenous studies. Markedly similar modifications in the major biological pathways between CKD and other chronic diseases supports shared deleterious molecular mechanisms producing muscle atrophy, irrespective of the underlying specific disease.

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