Role of OAS gene family in COVID-19 induced heart failure

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.

Abstract

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.

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