通过多个数据集探索哮喘的分子机制
2024/05/28
摘要
背景：哮喘是一种常见的慢性呼吸系统疾病，尽管我们的理解有了相当大的进步，但它仍然是一个谜。持续的努力发现新的分子靶点和全面了解其发病机制至关重要。
方法：在本研究中，我们分析了包括哮喘患者和健康对照在内的212个个体的基因表达数据，鉴定了267个差异表达基因，其中C1orf64和C7orf26被认为是哮喘发病的潜在关键基因。各种生物信息学工具，包括差异基因表达分析、途径富集、药物靶点预测和单细胞分析，被用来探索基因的潜在作用。
结果：定量PCR显示C1orf64和C7orf26在哮喘气道上皮组织中的差异表达，提示它们可能参与哮喘的发病机制。GSEA富集分析显示，这些基因在与哮喘进展相关的信号通路中显著富集，如ABC转运蛋白、细胞周期、CAMs、DNA复制和Notch信号通路。基于差异表达上调和下调的药物靶标预测强调了潜在的哮喘治疗，包括tyrphotin-ag-126、Cephalin、Verrucarin-a和Emetine。这些药物的选择是基于它们在分析中的意义以及它们已建立的抗炎和抗病毒侵袭特性。利用Seurat和Celldex软件包进行单细胞测序分析，揭示了疾病特异性基因表达模式和细胞类型。在T细胞、NK细胞和B细胞中观察到C1orf64和C7orf26的表达，有助于促进哮喘的标志性特征，表明它们对哮喘的发生和进展有潜在的影响。
结论：这项研究揭示了哮喘的新的遗传方面，突出了潜在的治疗途径。它体现了综合生物信息学在解码复杂疾病模式方面的力量。然而，这些发现需要进一步的验证，C1orf64和C7orf26在哮喘中的确切作用需要进一步的研究来验证它们的治疗潜力。
Exploring the molecular mechanisms of asthma across multiple datasets
L. S. Guo, E. H. Huang, T. T. Wang, Y. Ling and Z. Z. Li
Abstract
BACKGRUND:Asthma, a prevalent chronic respiratory disorder, remains enigmatic, notwithstanding considerable advancements in our comprehension. Continuous efforts are crucial for discovering novel molecular targets and gaining a comprehensive understanding of its pathogenesis.
METHODS:In this study, we analyzed gene expression data from 212 individuals, including asthma patients and healthy controls, to identify 267 differentially expressed genes, among which C1orf64 and C7orf26 emerged as potential key genes in asthma pathogenesis. Various bioinformatics tools, including differential gene expression analysis, pathway enrichment, drug target prediction, and single-cell analysis, were employed to explore the potential roles of the genes.
RESULTS:Quantitative PCR demonstrated differential expression of C1orf64 and C7orf26 in the asthmatic airway epithelial tissue, implying their potential involvement in asthma pathogenesis. GSEA enrichment analysis revealed significant enrichment of these genes in signaling pathways associated with asthma progression, such as ABC transporters, cell cycle, CAMs, DNA replication, and the Notch signaling pathway. Drug target prediction, based on upregulated and downregulated differential expression, highlighted potential asthma treatments, including Tyrphostin-AG-126, Cephalin, Verrucarin-a, and Emetine. The selection of these drugs was based on their significance in the analysis and their established anti-inflammatory and antiviral invasion properties. Utilizing Seurat and Celldex packages for single-cell sequencing analysis unveiled disease-specific gene expression patterns and cell types. Expression of C1orf64 and C7orf26 in T cells, NK cells, and B cells, instrumental in promoting hallmark features of asthma, was observed, suggesting their potential influence on asthma development and progression.
CONCLUSION:This study uncovers novel genetic aspects of asthma, highlighting potential therapeutic pathways. It exemplifies the power of integrative bioinformatics in decoding complex disease patterns. However, these findings require further validation, and the precise roles of C1orf64 and C7orf26 in asthma warrant additional investigation to validate their therapeutic potential.
背景：哮喘是一种常见的慢性呼吸系统疾病，尽管我们的理解有了相当大的进步，但它仍然是一个谜。持续的努力发现新的分子靶点和全面了解其发病机制至关重要。
方法：在本研究中，我们分析了包括哮喘患者和健康对照在内的212个个体的基因表达数据，鉴定了267个差异表达基因，其中C1orf64和C7orf26被认为是哮喘发病的潜在关键基因。各种生物信息学工具，包括差异基因表达分析、途径富集、药物靶点预测和单细胞分析，被用来探索基因的潜在作用。
结果：定量PCR显示C1orf64和C7orf26在哮喘气道上皮组织中的差异表达，提示它们可能参与哮喘的发病机制。GSEA富集分析显示，这些基因在与哮喘进展相关的信号通路中显著富集，如ABC转运蛋白、细胞周期、CAMs、DNA复制和Notch信号通路。基于差异表达上调和下调的药物靶标预测强调了潜在的哮喘治疗，包括tyrphotin-ag-126、Cephalin、Verrucarin-a和Emetine。这些药物的选择是基于它们在分析中的意义以及它们已建立的抗炎和抗病毒侵袭特性。利用Seurat和Celldex软件包进行单细胞测序分析，揭示了疾病特异性基因表达模式和细胞类型。在T细胞、NK细胞和B细胞中观察到C1orf64和C7orf26的表达，有助于促进哮喘的标志性特征，表明它们对哮喘的发生和进展有潜在的影响。
结论：这项研究揭示了哮喘的新的遗传方面，突出了潜在的治疗途径。它体现了综合生物信息学在解码复杂疾病模式方面的力量。然而，这些发现需要进一步的验证，C1orf64和C7orf26在哮喘中的确切作用需要进一步的研究来验证它们的治疗潜力。
（中日友好医院呼吸与危重症医学科 李春晓 摘译 林江涛 审校）
（Annals of Medicine 2024 Vol. 56 Issue 1 DOI: 10.1080/07853890.2023.2258926.）
（Annals of Medicine 2024 Vol. 56 Issue 1 DOI: 10.1080/07853890.2023.2258926.）
Exploring the molecular mechanisms of asthma across multiple datasets
L. S. Guo, E. H. Huang, T. T. Wang, Y. Ling and Z. Z. Li
Abstract
BACKGRUND:Asthma, a prevalent chronic respiratory disorder, remains enigmatic, notwithstanding considerable advancements in our comprehension. Continuous efforts are crucial for discovering novel molecular targets and gaining a comprehensive understanding of its pathogenesis.
METHODS:In this study, we analyzed gene expression data from 212 individuals, including asthma patients and healthy controls, to identify 267 differentially expressed genes, among which C1orf64 and C7orf26 emerged as potential key genes in asthma pathogenesis. Various bioinformatics tools, including differential gene expression analysis, pathway enrichment, drug target prediction, and single-cell analysis, were employed to explore the potential roles of the genes.
RESULTS:Quantitative PCR demonstrated differential expression of C1orf64 and C7orf26 in the asthmatic airway epithelial tissue, implying their potential involvement in asthma pathogenesis. GSEA enrichment analysis revealed significant enrichment of these genes in signaling pathways associated with asthma progression, such as ABC transporters, cell cycle, CAMs, DNA replication, and the Notch signaling pathway. Drug target prediction, based on upregulated and downregulated differential expression, highlighted potential asthma treatments, including Tyrphostin-AG-126, Cephalin, Verrucarin-a, and Emetine. The selection of these drugs was based on their significance in the analysis and their established anti-inflammatory and antiviral invasion properties. Utilizing Seurat and Celldex packages for single-cell sequencing analysis unveiled disease-specific gene expression patterns and cell types. Expression of C1orf64 and C7orf26 in T cells, NK cells, and B cells, instrumental in promoting hallmark features of asthma, was observed, suggesting their potential influence on asthma development and progression.
CONCLUSION:This study uncovers novel genetic aspects of asthma, highlighting potential therapeutic pathways. It exemplifies the power of integrative bioinformatics in decoding complex disease patterns. However, these findings require further validation, and the precise roles of C1orf64 and C7orf26 in asthma warrant additional investigation to validate their therapeutic potential.
上一篇：
Otulin的下调可诱导中性粒细胞型哮喘中的炎性小体活化
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肠凝集素-1基因的一种常见多态性对重度哮喘患者的黏液堵塞的影响
