Suppr超能文献

炎症细胞因子与创伤后应激障碍之间的因果关系:一项孟德尔随机化研究及潜在机制分析

Causal relationship between inflammatory cytokines and posttraumatic stress disorder: a Mendelian randomization study and potential mechanism analysis.

作者信息

Li Yingchong, Xu Bangliang, Chen Zhitao

机构信息

National Clinical Research Center for Child Health, The Children's Hospital, Zhejiang University School of Medicine, Hangzhou, People's Republic of China.

Shulan (Hangzhou) Hospital Affiliated to Zhejiang Shuren University Shulan International Medical College, Hangzhou, People's Republic of China.

出版信息

Eur J Psychotraumatol. 2025 Dec;16(1):2494480. doi: 10.1080/20008066.2025.2494480. Epub 2025 May 2.

Abstract

Post-traumatic stress disorder (PTSD) is a complex condition linked to inflammation. The causality between inflammatory cytokines and PTSD risk remains unclear. We conducted a bidirectional two-sample Mendelian randomization (MR) study using genome-wide association study (GWAS) data from 41 inflammatory cytokines and PTSD. Additional analyses included differential gene expression, protein-protein interaction, and functional enrichment to explore underlying mechanisms. MR analysis indicated that higher levels of stem cell factor (SCF) and interleukin-4 (IL-4) are associated with a reduced risk of PTSD. Genes POGZ and LRIG2 were identified as mediators, implicated in the TGF-beta signalling pathway. Our findings suggest a protective role of certain cytokines against PTSD and highlight potential molecular mediators. This knowledge could inform future therapeutic strategies for PTSD.

摘要

创伤后应激障碍(PTSD)是一种与炎症相关的复杂病症。炎性细胞因子与PTSD风险之间的因果关系仍不明确。我们使用来自41种炎性细胞因子和PTSD的全基因组关联研究(GWAS)数据进行了双向两样本孟德尔随机化(MR)研究。额外的分析包括差异基因表达、蛋白质-蛋白质相互作用和功能富集,以探索潜在机制。MR分析表明,干细胞因子(SCF)和白细胞介素-4(IL-4)水平较高与PTSD风险降低相关。基因POGZ和LRIG2被确定为介导因子,参与转化生长因子-β信号通路。我们的研究结果表明某些细胞因子对PTSD具有保护作用,并突出了潜在的分子介导因子。这些知识可为未来PTSD的治疗策略提供参考。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a783/12051613/7bed2cfe483a/ZEPT_A_2494480_F0001_OC.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验