Atherosclerosis (AS), a chronic inflammatory disease of the blood vessels, is the primary cause of cardiovascular disease, the leading cause of death worldwide. This study aimed to identify possible diagnostic markers for AS and determine their correlation with the infiltration of immune cells in AS. In total, 10 serum samples from AS patients and 10 samples from healthy subjects were collected. The original gene expression profiles of GSE43292 and GSE57691 were downloaded from the Gene Expression Omnibus database. Least absolute shrinkage and selection operator regression model and support vector machine recursive feature elimination analyses were carried out to identify candidate markers. The diagnostic values of the identified biomarkers were determined using receiver operating characteristic assays. The compositional patterns of the 22 types of immune cell fraction in AS were estimated using CIBERSORT. RT-PCR was performed to further determine the expression of the critical genes. This study identified 17 differentially expressed genes (DEGs) in AS samples. The identified DEGs were mainly involved in non-small cell lung carcinoma, pulmonary fibrosis, polycystic ovary syndrome, glucose intolerance, and T-cell leukemia. FHL5, IBSP, and SCRG1 have been identified as the diagnostic genes in AS. The expression of SCRG1 and FHL5 was distinctly downregulated in AS samples, and the expression of IBSP was distinctly upregulated in AS samples, which was further confirmed using our cohort by RT-PCR. Moreover, immune assays revealed that FHL5, IBSP, and SCRG1 were associated with several immune cells, such as CD8 T cells, naïve B cells, macrophage M0, activated memory CD4 T cells, and activated NK cells. Overall, future investigations into the occurrence and molecular mechanisms of AS may benefit from using the genes FHL5, IBSP, and SCRG1 as diagnostic markers for the condition.
Keywords: GEO datasets; atherosclerosis; biomarker; diagnosis; immune infiltration; machine learning.
Copyright © 2022 Ye, Wang, Lv, Wang and Cui.