Research Paper|Volume 13, Issue 9|pp 12733—12747

Identification of key pathways and genes in carotid atherosclerosis through bioinformatics analysis of RNA-seq data

Zhongchen Li¹, Jiheng Hao¹, Kun Chen¹, Qunlong Jiang¹, Peijian Wang¹, Xiaohui Xing¹, Jiyue Wang¹, Yinjiang Zhang², Yilei Xiao¹, Liyong Zhang¹

¹Department of Neurosurgery, Liaocheng People’s Hospital, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Liaocheng 252000, Shandong Province, P.R. China
²School of Pharmacy, Minzu University of China, Zhongguancun, Beijing 100081, P.R. China

* Equal contribution

Received: October 7, 2020Accepted: March 31, 2021Published: May 11, 2021

https://doi.org/10.18632/aging.202943

Copyright: © 2021 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

While acknowledging carotid atherosclerosis (CAS) as a risk factor for ischemic stroke, reports on its pathogenesis are scarce. This study aimed to explore the potential mechanism of CAS through RNA-seq data analysis. Carotid intima tissue samples from CAS patients and healthy subjects were subjected to RNA-seq analysis, which yielded, 1,427 differentially expressed genes (DEGs) related to CAS. Further, enrichment analysis (Gene Ontology, KEGG pathway, and MOCDE analysis) was performed on the DEGs. Hub genes identified via the protein-protein interaction network (PPI) were then analyzed using TRRUST, DisGeNET, PaGenBase, and CMAP databases. Results implicated inflammation and immunity in the pathogenesis of CAS. Also, lung disease was associated with CAS. Hub genes were expressed in multiple diseases, mainly regulated by RELA and NFKB1. Moreover, three small-molecule compounds were found via the CMAP database for management of CAS; hub genes served as potential targets. Collectively, inflammation and immunity are the potential pathological mechanisms of CAS. This study implicates CeForanide, Chenodeoxycholic acid, and 0317956-0000 as potential drug candidates for CAS treatment.