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研究脓毒症性心肌病发展中的免疫失调和枢纽基因。

Investigating immune dysregulation and hub genes in septic cardiomyopathy development.

机构信息

Emergency Trauma Center, The First Affiliated Hospital of Xinjiang Medical University, No. 137, Liyushan South Road, Urumqi, 830011, Xinjiang, People's Republic of China.

Department of Neurosurgery, Linyi People's Hospital, Linyi, People's Republic of China.

出版信息

Sci Rep. 2024 Sep 16;14(1):21608. doi: 10.1038/s41598-024-72724-1.

DOI:10.1038/s41598-024-72724-1
PMID:39294340
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11411067/
Abstract

Septic cardiomyopathy is a life-threatening heart dysfunction caused by severe infection. Considering the complexity of pathogenesis and high mortality, the identification of efficient biomarkers are needed to guide clinical practice. Based on multimicroarray analysis, this study aimed to explore the pathogenesis of septic cardiomyopathy and the related immune landscape. The results showed that septic cardiomyopathy resulted in organ dysfunction due to extreme pro- and anti-inflammatory effects. In this process, KLRG1, PRF1, BCL6, GAB2, MMP9, IL1R1, JAK3, IL6ST, and SERPINE1 were identified as the hub genes regulating the immune landscape of septic cardiomyopathy. Nine transcription factors regulated the expression of these genes: SRF, STAT1, SP1, RELA, PPARG, NFKB1, PPARA, SMAD3, and STAT3. The hub genes activated the Th17 cell differentiation pathway, JAK-STAT signaling pathway, and cytokine‒cytokine receptor interaction pathway. These pathways were mainly involved in regulating the inflammatory response, adaptive immune response, leukocyte-mediated immunity, cytokine-mediated immunity, immune effector processes, myeloid cell differentiation, and T-helper cell differentiation. These nine hub genes could be considered biomarkers for the early prediction of septic cardiomyopathy.

摘要

脓毒症性心肌病是一种由严重感染引起的危及生命的心功能障碍。鉴于其发病机制复杂和死亡率高，需要识别有效的生物标志物来指导临床实践。本研究基于多微阵列分析，旨在探讨脓毒症性心肌病的发病机制及相关免疫图谱。结果表明，脓毒症性心肌病导致器官功能障碍是由于极端的促炎和抗炎作用。在此过程中，KLRG1、PRF1、BCL6、GAB2、MMP9、IL1R1、JAK3、IL6ST 和 SERPINE1 被确定为调节脓毒症性心肌病免疫图谱的枢纽基因。9 个转录因子调节这些基因的表达：SRF、STAT1、SP1、RELA、PPARG、NFKB1、PPARA、SMAD3 和 STAT3。枢纽基因激活了 Th17 细胞分化途径、JAK-STAT 信号通路和细胞因子-细胞因子受体相互作用通路。这些通路主要参与调节炎症反应、适应性免疫反应、白细胞介素介导的免疫、细胞因子介导的免疫、免疫效应过程、髓样细胞分化和 T 辅助细胞分化。这 9 个枢纽基因可被视为脓毒症性心肌病早期预测的生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57b3/11411067/11ad37b625aa/41598_2024_72724_Fig7_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57b3/11411067/11ad37b625aa/41598_2024_72724_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57b3/11411067/0a0a99e69b4d/41598_2024_72724_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57b3/11411067/3f199a7a1a72/41598_2024_72724_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57b3/11411067/27f7980b7bf5/41598_2024_72724_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57b3/11411067/fee3c6727b2d/41598_2024_72724_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57b3/11411067/97542a4f69fb/41598_2024_72724_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57b3/11411067/11ad37b625aa/41598_2024_72724_Fig7_HTML.jpg

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