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通过加权基因协同表达网络分析和蛋白质-蛋白质相互作用网络构建,对毒症诱导的肌肉病的枢纽基因进行查

Jianhao Wang¹, Kun Han¹, Jinshuai Lu²

¹Postgraduate School, Xinjiang Medical University, Xinjiang, 830000, China.

BMC musculoskeletal disorders

|October 23, 2024

概括

败血症诱导的肌肉病导致肌肉缩和软弱. 这项研究确定了骨肌中的16个枢纽基因,为败血症诱导的肌肉病研究提供了潜在的生物标志物.

科学领域:

分子生物学分子生物学
遗传学是一个遗传学.
临界护理医学临界护理医学

背景情况:

败血症诱导的肌病是败血症的严重并发症,导致肌肉缩,软弱和再生能力受损.
病原发生涉及复杂的机制,如细胞因子作用和改变的蛋白质合成,但基因共同表达模式仍然不清楚.

研究的目的:

识别关键基因 (枢纽基因) 和参与败血症诱导肌病的信号通路.
探索败血症患者骨肌中的整体基因共同表达模式.

主要方法:

权重基因共同表达网络分析 (WGCNA) 应用于骨肌肉转录组数据,来自患有败血症引起的多器官衰竭的ICU患者.
从大约15181个基因中识别了共表达模块和枢纽基因.

主要成果:

确定了13个共同表达模块.
选择了16个枢纽基因 (3个上调,13个下调),包括FEM1B,KLHDC3,GPX3,NIFK,GNL2,EBNA1BP2,PES1,FBP2,PFKP,BYSL,HEATR1,WDR75,TBL3和WDR43.3等.
基因组丰富分析将这些基因与骨肌肉功能障碍,亡和亡联系起来.

结论:

已识别的16个枢纽基因是毒引起的肌肉病的潜在可靠生物标志物.
对这些基因的进一步研究可以促进对败血症引起的肌肉病的理解和治疗.

关键词:

基因组丰富分析 (GSEA) 是一种基因组丰富分析.蛋白质与蛋白质相互作用网络 (PPI)败血症这是一种败血症.败血症引起的肌肉病 (SIM)权重基因共同表达网络分析 (WGCNA)

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