铁死亡介导H1N1感染后细胞死亡的 可能病理机制研究

Possible Pathological Mechanism of Ferroptosis Mediated Cell Death after H1N1 Infection

目的:明确H1N1感染后铁死亡的机制,为H1N1的治疗提供新的思路。方法:本研究利用生物信息学,通过下载H1N1相关数据集GSE29385,进行差异基因分析,并与铁死亡相关基因取交集后,做GO、KEGG分析,并构建PPI网络及筛选关键基因,阐明铁死亡在H1N1病理发展过程中的可能机制。结果:GO分析及KEGG分析提示铁死亡与H1N1感染后脂质过氧化相关,其中mTOR信号通路可能发挥主要作用。结论:H1N1感染后mTOR信号通路途径激活,铁死亡增加,并导致线粒体中脂质过氧化,从而导致H1N1感染后细胞死亡。

Objective:Clarify the mechanism of ferroptosis after H1N1 infection and provide new ideas for the treatment of H1N1.Methods:We used bioinformatics methods to download H1N1-related datasets and GSE29385 to analyze differential genes,and intersected with ferroptosis-related genes for GO and KEGG analysis,and constructed PPI networks and screened key genes to elucidate the possible mechanism of ferroptosis in the pathological development of H1N1.Results:GO analysis and KEGG analysis showed that ferroptosis was associated with lipid peroxidation after H1N1 infection,and the mTOR signaling pathway may play a major role.Conclusion:After H1N1 infection,the mTOR signaling pathway is activated,ferrcrosis is increased,and lipid peroxidation in mitochondria is led,which leads to cell death after H1N1 infection.