Postgraduate School, Xinjiang Medical University, Xinjiang, 830000, China.
Department of Emergency, People's Hospital of Xinjiang Uygur Autonomous Region, No 91, Tian Chi Road, Xinjiang, 830001, China.
BMC Musculoskelet Disord. 2024 Oct 22;25(1):834. doi: 10.1186/s12891-024-07967-0.
Sepsis-induced myopathy is one of the serious complications of sepsis, which severely affects the respiratory and peripheral motor systems of patients, reduces their quality of life, and jeopardizes their lives, as evidenced by muscle atrophy, loss of strength, and impaired regeneration after injury. The pathogenesis of sepsis-induced myopathy is complex, mainly including cytokine action, enhances free radical production in muscle, increases muscle protein hydrolysis, and decreases skeletal muscle protein synthesis, etc. The above mechanisms have been demonstrated in existing studies. However, it is still unclear how the overall pattern of gene co-expression affects the pathological process of sepsis-induced myopathy. Therefore, we intend to identify hub genes and signaling pathways. Weighted gene co-expression network analysis was our main approach to study gene expression profiles: skeletal muscle transcriptome in ICU patients with sepsis-induced multi-organ failure (GSE13205). After data pre-processing, about 15,181 genes were used to identify 13 co-expression modules. Then, 16 genes (FEM1B, KLHDC3, GPX3, NIFK, GNL2, EBNA1BP2, PES1, FBP2, PFKP, BYSL, HEATR1, WDR75, TBL3, and WDR43) were selected as the hub genes including 3 up-regulated genes and 13 down-regulated genes. Then, Gene Set Enrichment Analysis was performed to show that the hub genes were closely associated with skeletal muscle dysfunction, necrotic and apoptotic skeletal myoblasts, and apoptosis in sepsis-induced myopathy. Overall, 16 candidate biomarkers were certified as reliable features for more in-depth exploration of sepsis-induced myopathy in basic and clinical studies.
脓毒症相关性肌病是脓毒症的严重并发症之一，严重影响患者的呼吸和周围运动系统，降低生活质量，危及生命，其特征为肌肉萎缩、肌力丧失和损伤后再生受损。脓毒症相关性肌病的发病机制复杂，主要包括细胞因子作用、增强肌肉中自由基的产生、增加肌肉蛋白水解和减少骨骼肌蛋白合成等。现有研究已经证实了上述机制。然而，整体基因共表达模式如何影响脓毒症相关性肌病的病理过程仍不清楚。因此，我们旨在确定枢纽基因和信号通路。加权基因共表达网络分析是我们研究基因表达谱的主要方法：脓毒症诱导多器官衰竭 ICU 患者的骨骼肌转录组（GSE13205）。在数据预处理后，使用约 15181 个基因来识别 13 个共表达模块。然后，选择 16 个基因（FEM1B、KLHDC3、GPX3、NIFK、GNL2、EBNA1BP2、PES1、FBP2、PFKP、BYSL、HEATR1、WDR75、TBL3 和 WDR43）作为枢纽基因，包括 3 个上调基因和 13 个下调基因。然后，进行基因集富集分析表明，枢纽基因与脓毒症相关性肌病中的骨骼肌功能障碍、坏死和凋亡成肌细胞以及细胞凋亡密切相关。总的来说，16 个候选生物标志物被证明是深入探索脓毒症相关性肌病的可靠特征，可用于基础和临床研究。
