Wang Jing, Xiang Yaoxian, Wu Lihui, Zhang Chan, Han Baojuan, Cheng Yurong, Tong Yingying, Yan Dong, Wang Li
Department of Oncology, Beijing Luhe hospital Affiliated to Capital Medical University, 101149, Beijing, China.
Zhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310006, Zhejiang, China.
Eur J Clin Nutr. 2024 Dec;78(12):1032-1040. doi: 10.1038/s41430-024-01486-w. Epub 2024 Aug 9.
Sarcopenia is among the most common musculoskeletal illnesses, yet its underlying biochemical mechanisms remain incompletely understood. Identifying the relationship of inflammatory cytokines with sarcopenia components would help understand the etiology of sarcopenia. We performed a bi-directional Mendelian randomization study to explore the causal relationship between 41 inflammatory cytokines and sarcopenia-related traits.
The study was performed in two stages using bidirectional dual-sample Mendelian randomization. We obtained aggregated statistical data on inflammatory factors, low grip strength, and ALM from genome-wide association studies. To explore the causal association between exposure and outcomes, we primarily utilized the inverse variance weighted strategy. Furthermore, we conducted sensitivity analyses through the use of Mendelian randomization (MR) Egger, weighted median and simple mode methods. To evaluate robustness of the results and to identify and adjust for horizontal pleiotropy, we performed the MR Pleiotropy RESidual Sum and Outlier test, the MR Egger intercept test, and a leave-one-out analysis.
The results displayed a potential association between interleukin-10 (OR: 1.046, 95% CI: 1.002-1.093, p = 0.042) and vascular endothelial growth factor (OR: 1.024, 95% CI: 1.001-1.047, p = 0.038) and the risk of low hand-grip strength. Moreover, interferon gamma-induced protein 10 (OR: 1.010, 95% CI: 1.000-1.019, p = 0.042) and macrophage colony-stimulating factor (OR: 1.010, 95% CI: 1.003-1.017, p = 0.003) were significantly linked to a higher risk of ALM.
We identified a causal relationship between multiple inflammatory factors and sarcopenia-related traits. Our study offers valuable insights into innovative methods for the sarcopenia prevention and treatment by regulating inflammatory factors.
肌肉减少症是最常见的肌肉骨骼疾病之一，但其潜在的生化机制仍未完全了解。确定炎症细胞因子与肌肉减少症各组成部分之间的关系将有助于理解肌肉减少症的病因。我们进行了一项双向孟德尔随机化研究，以探讨41种炎症细胞因子与肌肉减少症相关特征之间的因果关系。
本研究分两个阶段使用双向双样本孟德尔随机化进行。我们从全基因组关联研究中获得了关于炎症因子、低握力和四肢肌肉量的汇总统计数据。为了探讨暴露与结局之间的因果关联，我们主要采用逆方差加权策略。此外，我们通过使用孟德尔随机化（MR）Egger法、加权中位数法和简单模式法进行敏感性分析。为了评估结果的稳健性并识别和调整水平多效性，我们进行了MR多效性残差和异常值检验、MR Egger截距检验以及留一法分析。
结果显示白细胞介素-10（OR：1.046，95%CI：1.002-1.093，p = 0.042）和血管内皮生长因子（OR：1.024，95%CI：1.001-1.047，p = 0.038）与低握力风险之间存在潜在关联。此外，干扰素γ诱导蛋白10（OR：1.010，95%CI：1.000-1.019，p = 0.042）和巨噬细胞集落刺激因子（OR：1.010，95%CI：1.003-1.017，p = 0.003）与四肢肌肉量较高风险显著相关。
我们确定了多种炎症因子与肌肉减少症相关特征之间的因果关系。我们的研究为通过调节炎症因子预防和治疗肌肉减少症的创新方法提供了有价值的见解。
