Data driven analysis reveals prognostic genes and immunological targets in human sepsis-associated acute kidney injury.

IF 2.6 3区 医学 Q1 EMERGENCY MEDICINE
Qing Zhao, Jinfu Ma, Jianguo Xiao, Zhe Feng, Hui Liu
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引用次数: 0

Abstract

Background: The molecular mechanism of sepsis-associated acute kidney injury (SA-AKI) is unclear. We analyzed co-differentially expressed genes (co-DEGs) to elucidate the underlying mechanism and intervention targets of SA-AKI.

Methods: The microarray datasets GSE65682, GSE30718, and GSE174220 were downloaded from the Gene Expression Omnibus (GEO) database. We identified the co-DEGs and constructed a gene co-expression network to screen the hub genes. We analyzed immune correlations and disease correlations and performed functional annotation of the hub genes. We also performed single-cell and microenvironment analyses and investigated the enrichment pathways and the main transcription factors. Finally, we conducted a correlation analysis to evaluate the role of the hub genes.

Results: Interleukin 32 (IL32) was identified as the hub gene in SA-AKI, and the main enriched signaling pathways were associated with hemopoiesis, cellular response to cytokine stimulus, inflammatory response, and regulation of kidney development. Additionally, IL32 was significantly associated with mortality in SA-AKI patients. Monocytes, macrophages, T cells, and NK cells were closely related to IL32 and were involved in the immune microenvironment in SA-AKI patients. IL32 expression increased significantly in the kidney of septic mouse. Toll-like receptor 2 (TLR2) was significantly and negatively correlated with IL32.

Conclusion: IL32 is the key gene involved in SA-AKI and is significantly associated with prognosis. TLR2 and relevant immune cells are closely related to key genes.

数据驱动分析揭示了人类脓毒症相关急性肾损伤的预后基因和免疫学靶标。
背景:脓毒症相关急性肾损伤(SA-AKI)的分子机制尚不清楚。我们分析了共差异表达基因(co-DEGs),以阐明脓毒症相关急性肾损伤(SA-AKI)的潜在机制和干预靶点:方法:我们从基因表达总库(GEO)数据库下载了 GSE65682、GSE30718 和 GSE174220 微阵列数据集。我们确定了共DEGs,并构建了基因共表达网络以筛选枢纽基因。我们分析了免疫相关性和疾病相关性,并对枢纽基因进行了功能注释。我们还进行了单细胞和微环境分析,研究了富集途径和主要转录因子。最后,我们进行了相关性分析,以评估中心基因的作用:结果:白细胞介素32(IL32)被确定为SA-AKI的枢纽基因,主要的富集信号通路与造血、细胞对细胞因子刺激的反应、炎症反应和肾脏发育调控有关。此外,IL32与SA-AKI患者的死亡率显著相关。单核细胞、巨噬细胞、T细胞和NK细胞与IL32密切相关,并参与了SA-AKI患者的免疫微环境。IL32在败血症小鼠肾脏中的表达明显增加。Toll样受体2(TLR2)与IL32呈显著负相关:结论:IL32是参与SA-AKI的关键基因,与预后密切相关。结论:IL32是参与SA-AKI的关键基因,与预后密切相关。
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来源期刊
CiteScore
2.50
自引率
28.60%
发文量
671
期刊介绍: The journal will cover technical, clinical and bioengineering studies related to multidisciplinary specialties of emergency medicine, such as cardiopulmonary resuscitation, acute injury, out-of-hospital emergency medical service, intensive care, injury and disease prevention, disaster management, healthy policy and ethics, toxicology, and sudden illness, including cardiology, internal medicine, anesthesiology, orthopedics, and trauma care, and more. The journal also features basic science, special reports, case reports, board review questions, and more. Editorials and communications to the editor explore controversial issues and encourage further discussion by physicians dealing with emergency medicine.
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