整合分子相互作用和基因表达，以鉴定慢性阻塞性肺疾病的生物标志物和网络模块。
Integrating molecular interactions and gene expression to identify biomarkers and network modules of chronic obstructive pulmonary disease.
机构信息
Faculty of Information Technology, Macau University of Science and Technology, Macau, China.
Macau Institute of Systems Engineering and Collaborative Laboratory of Intelligent Science and Systems, Macau University of Science and Technology, Macau, China.
出版信息
Technol Health Care. 2022;30(S1):135-142. doi: 10.3233/THC-228013.
BACKGROUND
Chronic obstructive pulmonary disease (COPD) causes chronic obstructive conditions, chronic bronchitis, and emphysema, and is a major cause of death worldwide. Although several efforts for identifying biomarkers and pathways have been made, specific causal COPD mechanism remains unknown.
OBJECTIVE
This study combined biological interaction data with gene expression data for a better understanding of the biological process and network module for COPD.
METHODS
Using a sparse network-based method, we selected 49 genes from peripheral blood mononuclear cell expression data of 136 subjects, including 42 ex-smoking controls and 94 subjects with COPD.
RESULTS
These 49 genes might influence biological processes and molecular functions related to COPD. For example, our result suggests that FoxO signaling may contribute to the atrophy of COPD peripheral muscle tissues via oxidative stress.
CONCLUSIONS
Our approach enhances the existing understanding of COPD disease pathogenesis and predicts new genetic markers and pathways that may influence COPD pathogenesis.
背景
慢性阻塞性肺疾病（COPD）导致慢性阻塞性疾病、慢性支气管炎和肺气肿，是全球主要的死亡原因。尽管已经有许多努力用于识别生物标志物和途径，但特定的 COPD 发病机制仍不清楚。
目的
本研究将生物相互作用数据与基因表达数据相结合，以更好地了解 COPD 的生物学过程和网络模块。
方法
使用稀疏网络基方法，我们从 136 名受试者的外周血单核细胞表达数据中选择了 49 个基因，其中包括 42 名戒烟对照者和 94 名 COPD 患者。
结果
这 49 个基因可能影响与 COPD 相关的生物学过程和分子功能。例如，我们的结果表明，FoxO 信号通路可能通过氧化应激导致 COPD 外周肌肉组织萎缩。
结论
我们的方法增强了对 COPD 发病机制的现有理解，并预测了可能影响 COPD 发病机制的新的遗传标记和途径。
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