Exploring shared biomarkers and shared pathways in insomnia and atherosclerosis using integrated bioinformatics analysis.

IF 3.5 3区医学 Q2 NEUROSCIENCES Frontiers in Molecular Neuroscience Pub Date : 2024-10-08 eCollection Date: 2024-01-01 DOI:10.3389/fnmol.2024.1477903

Qichong Yang, Juncheng Liu, Tingting Zhang, Tingting Zhu, Siyu Yao, Rongzi Wang, Wenjuan Wang, Haliminai Dilimulati, Junbo Ge, Songtao An

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Abstract

Background: Insomnia (ISM) is one of the non-traditional drivers of atherosclerosis (AS) and an important risk factor for AS-related cardiovascular disease. Our study aimed to explore the shared pathways and diagnostic biomarkers of ISM-related AS using integrated bioinformatics analysis.

Methods: We download the datasets from the Gene Expression Omnibus database and the GeneCards database. Weighted gene co-expression network analysis and gene differential expression analysis were applied to screen the AS-related gene set. The shared genes of ISM and AS were obtained by intersecting with ISM-related genes. Subsequently, candidate diagnostic biomarkers were identified by constructing protein-protein interaction networks and machine learning algorithms, and a nomogram was constructed. Moreover, to explore potential mechanisms, a comprehensive analysis of shared genes was carried out, including enrichment analysis, protein interactions, immune cell infiltration, and single-cell sequencing analysis.

Results: We successfully screened 61 genes shared by ISM and AS, of which 3 genes (IL10RA, CCR1, and SPI1) were identified as diagnostic biomarkers. A nomogram with excellent predictive value was constructed (the area under curve of the model constructed by the biomarkers was 0.931, and the validation set was 0.745). In addition, the shared genes were mainly enriched in immune and inflammatory response regulation pathways. The biomarkers were associated with a variety of immune cells, especially myeloid immune cells.

Conclusion: We constructed a diagnostic nomogram based on IL10RA, CCR1, and SPI1 and explored the inflammatory-immune mechanisms, which indicated new insights for early diagnosis and treatment of ISM-related AS.

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利用综合生物信息学分析探索失眠和动脉粥样硬化中的共享生物标志物和共享途径。

背景：失眠（ISM）是动脉粥样硬化（AS）的非传统驱动因素之一，也是AS相关心血管疾病的重要危险因素。我们的研究旨在利用综合生物信息学分析探索与失眠相关的强直性脊柱炎的共享途径和诊断生物标志物：方法：我们从基因表达总库（Gene Expression Omnibus）数据库和基因卡片（GeneCards）数据库下载数据集。方法：我们从基因表达总库（Gene Expression Omnibus）和基因卡片（GeneCards）数据库中下载数据集，应用加权基因共表达网络分析和基因差异表达分析法筛选强直性脊柱炎相关基因。通过与ISM相关基因的交叉，得到ISM和AS的共有基因。随后，通过构建蛋白质-蛋白质相互作用网络和机器学习算法，确定了候选诊断生物标志物，并构建了提名图。此外，为了探索潜在的机制，我们还对共有基因进行了综合分析，包括富集分析、蛋白质相互作用、免疫细胞浸润和单细胞测序分析：结果：我们成功筛选出61个ISM和AS共有基因，其中3个基因（IL10RA、CCR1和SPI1）被确定为诊断生物标志物。研究还构建了一个具有极高预测价值的提名图（由生物标志物构建的模型的曲线下面积为 0.931，验证集为 0.745）。此外，共享基因主要富集在免疫和炎症反应调节通路中。这些生物标志物与多种免疫细胞有关，尤其是髓系免疫细胞：我们构建了基于 IL10RA、CCR1 和 SPI1 的诊断提名图，并探索了炎症-免疫机制，为 ISM 相关强直性脊柱炎的早期诊断和治疗提供了新的思路。

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来源期刊

Frontiers in Molecular Neuroscience NEUROSCIENCES-

CiteScore

5.70

自引率

2.10%

发文量

669

审稿时长

14 weeks

期刊介绍： Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and function of the brain across all levels. The scope of our journal encompasses synaptic and cellular proteins, coding and non-coding RNA, and molecular mechanisms regulating cellular and dendritic RNA translation. In recent years, a plethora of new cellular and synaptic players have been identified from reduced systems, such as neuronal cultures, but the relevance of these molecules in terms of cellular and synaptic function and plasticity in the living brain and its circuits has not been validated. The effects of spine growth and density observed using gene products identified from in vitro work are frequently not reproduced in vivo. Our journal is particularly interested in studies on genetically engineered model organisms (C. elegans, Drosophila, mouse), in which alterations in key molecules underlying cellular and synaptic function and plasticity produce defined anatomical, physiological and behavioral changes. In the mouse, genetic alterations limited to particular neural circuits (olfactory bulb, motor cortex, cortical layers, hippocampal subfields, cerebellum), preferably regulated in time and on demand, are of special interest, as they sidestep potential compensatory developmental effects.