Department of Biotechnology, Delhi Technological University (DTU), Delhi, 110042, India.
Med Biol Eng Comput. 2024 Aug;62(8):2557-2570. doi: 10.1007/s11517-024-03099-8. Epub 2024 Apr 22.
Combined pulmonary fibrosis and emphysema (CPFE) presents a unique challenge in respiratory disorders, merging features of interstitial lung disease (ILD) and chronic obstructive pulmonary disease (COPD). Using the random forest algorithm, our study thoroughly examines the molecular details of CPFE. Analyzing gene expression datasets from GSE47460 (ILD: 254, COPD: 220, control: 108), we identify key genes namely ADRB2, CDH3, IRS2, MATN3, CD38, PDIA4, VEGFC, and among twenty others, crucial in airway regulation, lung function, and apoptosis, shaping the complex pathogenesis of CPFE. Additionally, miRNAs (hsa-mir-101-3p, hsa-mir-1343-3p, hsa-mir-27a-3p, and miR-16-5p) showcase regulatory impacts on CPFE-related molecular pathways. Our machine learning model unveils these intricate interactions, offering a comprehensive insight into CPFE's molecular mechanisms. This research not only pinpoints potential therapeutic targets and biomarkers but also opens avenues for innovative approaches in managing CPFE, linking ILD and COPD within this complex respiratory condition.
合并性肺纤维化和肺气肿(CPFE)在呼吸紊乱中提出了独特的挑战,合并了肺间质疾病(ILD)和慢性阻塞性肺疾病(COPD)的特征。本研究使用随机森林算法深入研究了 CPFE 的分子细节。通过分析 GSE47460 中的基因表达数据集(ILD:254,COPD:220,对照:108),我们确定了关键基因,即 ADRB2、CDH3、IRS2、MATN3、CD38、PDIA4、VEGFC 以及其他二十个基因,这些基因在气道调节、肺功能和细胞凋亡中起着关键作用,塑造了 CPFE 的复杂发病机制。此外,miRNA(hsa-mir-101-3p、hsa-mir-1343-3p、hsa-mir-27a-3p 和 miR-16-5p)展示了对 CPFE 相关分子途径的调节影响。我们的机器学习模型揭示了这些复杂的相互作用,为 CPFE 的分子机制提供了全面的见解。这项研究不仅确定了潜在的治疗靶点和生物标志物,还为管理 CPFE 提供了新的途径,将ILD 和 COPD 联系在这一复杂的呼吸系统疾病中。