Role of OAS gene family in COVID-19 induced heart failure
Related Experiment Video
Updated: Aug 6, 2025

Viral Transgene Expression in Rodent Hearts and the Assessment of Cardiac Arrhythmia Risk
Published on: July 27, 2022
Li-Juan Gao1, Zhong-Mei He2, Yi-Ying Li2
1Key Laboratory of Cellular Physiology, Department of Physiology, Ministry of Education, Shanxi Medical University, Taiyuan, 030001, Shanxi, People's Republic of China. gaolijuan@sxmu.edu.cn.
Background:
COVID-19, the current global pandemic caused by SARS-CoV-2 infection, can damage the heart and lead to heart failure (HF) and even cardiac death. The 2',5'-oligoadenylate synthetase (OAS) gene family encode interferon (IFN)-induced antiviral proteins which is associated with the antiviral immune responses of COVID-19. While the potential association of OAS gene family with cardiac injury and failure in COVID-19 has not been determined.
Methods:
The expression levels and biological functions of OAS gene family in SARS-CoV-2 infected cardiomyocytes dataset (GSE150392) and HF dataset (GSE120852) were determined by comprehensive bioinformatic analysis and experimental validation. The associated microRNAs (miRNAs) were explored from Targetscan and GSE104150. The potential OAS gene family-regulatory chemicals or ingredients were predicted using Comparative Toxicogenomics Database (CTD) and SymMap database.
Results:
The OAS genes were highly expressed in both SARS-CoV-2 infected cardiomyocytes and failing hearts. The differentially expressed genes (DEGs) in the two datasets were enriched in both cardiovascular disease and COVID-19 related pathways. The miRNAs-target analysis indicated that 10 miRNAs could increase the expression of OAS genes. A variety of chemicals or ingredients were predicted regulating the expression of OAS gene family especially estradiol.
Conclusion:
OAS gene family is an important mediator of HF in COVID-19 and may serve as a potential therapeutic target for cardiac injury and HF in COVID-19.
Insights
The 2
Area of Science:
- Cardiology
- Virology
- Immunology
Background:
- COVID-19 (SARS-CoV-2) infection can cause cardiac damage, leading to heart failure (HF).
- The 2',5'-oligoadenylate synthetase (OAS) gene family plays a role in antiviral immune responses.
- The association between OAS genes and COVID-19-related cardiac injury was previously undetermined.
Purpose of the Study:
- To investigate the expression and function of OAS gene family in COVID-19-associated cardiac injury.
- To explore regulatory mechanisms including microRNAs and chemicals impacting OAS gene expression in heart failure.
Main Methods:
- Bioinformatic analysis of SARS-CoV-2 infected cardiomyocytes (GSE150392) and heart failure (GSE120852) datasets.
- Experimental validation of OAS gene expression and function.
- Analysis of microRNA targets and prediction of regulatory chemicals using databases like CTD and SymMap.
Main Results:
- OAS genes were highly expressed in both infected cardiomyocytes and failing hearts.
- Enrichment analysis revealed associations with cardiovascular disease and COVID-19 pathways.
- Ten microRNAs were identified as potential regulators of OAS gene expression, with estradiol predicted as a key regulatory chemical.
Conclusions:
- The OAS gene family is implicated as a mediator of heart failure in COVID-19 patients.
- OAS genes represent a potential therapeutic target for managing cardiac injury and heart failure in COVID-19.
Related Concept Videos
Heart Failure II: Pathophysiology
Pathophysiology of Heart Failure
Pulmonary Hypertension: Classification and Pathogenesis
There are various classifications for PH, each relating to different underlying causes and also...
Coronary Artery Disease II: Pathophysiology
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Cardiomyopathy III: Hypertrophic Cardiomyopathy

