Molecular Mechanisms of Cardiac Injury Associated With Myocardial SARS-CoV-2 Infection

Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread around the world. The development of cardiac injury is a common condition in patients with COVID-19, but the pathogenesis remains unclear. The RNA-Seq dataset (GSE150392) comparing e...

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Main Authors: Xianfang Liu, Longquan Lou, Lei Zhou
Format: Article
Language:English
Published: Frontiers Media S.A. 2022-01-01
Series:Frontiers in Cardiovascular Medicine
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fcvm.2021.643958/full
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author Xianfang Liu
Longquan Lou
Lei Zhou
author_facet Xianfang Liu
Longquan Lou
Lei Zhou
author_sort Xianfang Liu
collection DOAJ
description Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread around the world. The development of cardiac injury is a common condition in patients with COVID-19, but the pathogenesis remains unclear. The RNA-Seq dataset (GSE150392) comparing expression profiling of mock human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and SARS-CoV-2-infected hiPSC-CMs was obtained from Gene Expression Omnibus (GEO). We identified 1,554 differentially expressed genes (DEGs) based on GSE150392. Gene set enrichment analysis (GSEA), Gene ontology (GO) analysis, and Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis showed that immune-inflammatory responses were activated by SARS-CoV-2, while muscle contraction, cellular respiration, and cell cycle of hiPSC-CMs were inhibited. A total of 15 hub genes were identified according to protein–protein interaction (PPI), among which 11 upregulated genes were mainly involved in cytokine activation related to the excessive inflammatory response. Moreover, we identified potential drugs based on these hub genes. In conclusion, SARS-CoV-2 infection of cardiomyocytes caused a strong defensive response, leading to excessive immune inflammation, cell hypoxia, functional contractility reduction, and apoptosis, ultimately resulting in myocardial injury.
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spelling doaj.art-51e195387be34a0f9b880eccd8db1c632022-12-21T21:20:48ZengFrontiers Media S.A.Frontiers in Cardiovascular Medicine2297-055X2022-01-01810.3389/fcvm.2021.643958643958Molecular Mechanisms of Cardiac Injury Associated With Myocardial SARS-CoV-2 InfectionXianfang Liu0Longquan Lou1Lei Zhou2Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, ChinaDepartment of General Surgery, The Third People's Hospital of Hangzhou, Hangzhou, ChinaDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, ChinaCoronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread around the world. The development of cardiac injury is a common condition in patients with COVID-19, but the pathogenesis remains unclear. The RNA-Seq dataset (GSE150392) comparing expression profiling of mock human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and SARS-CoV-2-infected hiPSC-CMs was obtained from Gene Expression Omnibus (GEO). We identified 1,554 differentially expressed genes (DEGs) based on GSE150392. Gene set enrichment analysis (GSEA), Gene ontology (GO) analysis, and Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis showed that immune-inflammatory responses were activated by SARS-CoV-2, while muscle contraction, cellular respiration, and cell cycle of hiPSC-CMs were inhibited. A total of 15 hub genes were identified according to protein–protein interaction (PPI), among which 11 upregulated genes were mainly involved in cytokine activation related to the excessive inflammatory response. Moreover, we identified potential drugs based on these hub genes. In conclusion, SARS-CoV-2 infection of cardiomyocytes caused a strong defensive response, leading to excessive immune inflammation, cell hypoxia, functional contractility reduction, and apoptosis, ultimately resulting in myocardial injury.https://www.frontiersin.org/articles/10.3389/fcvm.2021.643958/fullCOVID-19cardiac injurySARS-CoV-2RNA-Seqbioinformatics analysis
spellingShingle Xianfang Liu
Longquan Lou
Lei Zhou
Molecular Mechanisms of Cardiac Injury Associated With Myocardial SARS-CoV-2 Infection
Frontiers in Cardiovascular Medicine
COVID-19
cardiac injury
SARS-CoV-2
RNA-Seq
bioinformatics analysis
title Molecular Mechanisms of Cardiac Injury Associated With Myocardial SARS-CoV-2 Infection
title_full Molecular Mechanisms of Cardiac Injury Associated With Myocardial SARS-CoV-2 Infection
title_fullStr Molecular Mechanisms of Cardiac Injury Associated With Myocardial SARS-CoV-2 Infection
title_full_unstemmed Molecular Mechanisms of Cardiac Injury Associated With Myocardial SARS-CoV-2 Infection
title_short Molecular Mechanisms of Cardiac Injury Associated With Myocardial SARS-CoV-2 Infection
title_sort molecular mechanisms of cardiac injury associated with myocardial sars cov 2 infection
topic COVID-19
cardiac injury
SARS-CoV-2
RNA-Seq
bioinformatics analysis
url https://www.frontiersin.org/articles/10.3389/fcvm.2021.643958/full
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