Machine Learning-Driven Discovery of TRIM Genes as Diagnostic Biomarkers for Idiopathic Pulmonary Fibrosis

利用机器学习发现TRIM基因作为特发性肺纤维化的诊断生物标志物

阅读:1

Abstract

BACKGROUND Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with limited effective treatments and significant challenges in early diagnosis. Identifying reliable biomarkers is crucial for improving diagnostic accuracy and patient outcomes. MATERIAL AND METHODS We analyzed TRIM family gene expression in IPF patients and healthy controls using GSE93606, GSE33566, and GSE38958 datasets. Consensus clustering and WGCNA identified IPF subtypes and hub genes. Machine learning models (RF, GLM, SVM, XGB) were built to identify key disease genes. A nomogram for clinical prediction was developed and validated. Peripheral blood samples from IPF patients and healthy controls were used to validate gene expression via qPCR. RESULTS TRIM family genes were significantly differentially expressed between IPF patients and healthy controls. Two distinct IPF subtypes (C1 and C2) were identified, each exhibiting unique biological functions and signaling pathways. The RF model outperformed other machine learning models, identifying TNIK, NCL, ROPN1L, MTR, and HNRNPH1 as key disease-characteristic genes. The nomogram demonstrated good predictive accuracy (AUC: 0.741, 95% CI: 0.556-0.897). qPCR validation confirmed increased expression of 4 genes in IPF patients, except for ROPN1L, which showed decreased expression. CONCLUSIONS This study identifies and validates TRIM family genes as potential biomarkers for IPF diagnosis using clinical samples. The findings support the integration of these biomarkers into diagnostic workflows, potentially enhancing early diagnosis and personalized treatment strategies for IPF patients. Further research is needed to explore the prognostic value and underlying mechanisms of these genes.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。