ArticleFrontiers in cardiovascular medicine2022
Bioinformatics approach to identify the influences of SARS-COV2 infections on atherosclerosis.
Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- The physiological effects of APOE genotype in healthy young/middle-aged individuals.Biological reviews of the Cambridge Philosophical Society · 2026Article
- From Systemic Inflammation to Vascular Remodeling: Investigating Carotid IMT in COVID-19 Survivors.Viruses · 2025Article
- PROS1 released by lung basal cells limits inflammation in epithelial and monocytes during SARS-CoV-2 infection.Discovery immunology · 2025Article
- A Multi-Machine Learning Consensus Model Based on Clinical Features Reveals That Interleukin-10 Derived from Monocytes Leads to a Poor Prognosis in Patients with Coronavirus Disease-2019.Journal of inflammation research · 2024Article
- Identification of Gene Markers Associated with COVID-19 Severity and Recovery in Different Immune Cell Subtypes.Biology · 2023Article
- Complement and COVID-19: Three years on, what we know, what we don't know, and what we ought to know.Immunobiology · 2023Review
- Bioinformatics and system biology approach to identify the influences of SARS-CoV-2 on metabolic unhealthy obese patients.Frontiers in molecular biosciences · 2023Article
- Identification and validation of hub genes involved in foam cell formation and atherosclerosis developmentPeerJ · 2023Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coronavirus disease (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been a global pandemic since early 2020. Understanding the relationship between various systemic disease and COVID-19 through disease ontology (DO) analysis, an approach based on disease similarity studies, has found that COVID-19 is most strongly associated with atherosclerosis. The study provides new insights for the common pathogenesis of COVID-19 and atherosclerosis by looking for common transcriptional features. Two datasets (GSE152418 and GSE100927) were downloaded from GEO database to search for common differentially expressed genes (DEGs) and shared pathways. A total of 34 DEGs were identified. Among them, ten hub genes with high degrees of connectivity were picked out, namely C1QA, C1QB, C1QC, CD163, SIGLEC1, APOE, MS4A4A, VSIG4, CCR1 and STAB1. This study suggests the critical role played by Complement and coagulation cascades in COVID-19 and atherosclerosis. Our findings underscore the importance of C1q in the pathogenesis of COVID-19 and atherosclerosis. Activation of the complement system can lead to endothelial dysfunction. The DEGs identified in this study provide new biomarkers and potential therapeutic targets for the prevention of atherosclerosis.
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Registered trials
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