Abstract

Background: Coronavirus disease 2019 (COVID-19) is a viral respiratory illness caused by the novel coronavirus SARS-CoV-2. The presence of the pre-existing cardiac disease is associated with an increased likelihood of severe clinical course and mortality in patients with COVID-19. Besides, current evidence indicates that a significant number of patients with COVID-19 also exhibit cardiovascular involvement even in the absence of known cardiac risk factors. Therefore, there is a need to understand the underlying mechanisms and genetic predispositions that explain cardiovascular involvement in COVID-19.Objectives: In silico analysis of publicly available datasets to decipher the molecular basis, potential pathways, and the role of the endothelium in the pathogenesis of cardiac and vascular injuries in COVID-19.Materials and Methods: Consistent significant differentially expressed genes (DEGs) shared by endothelium and peripheral immune cells were identified in five microarray transcriptomic profiling datasets in patients with venous thromboembolism “VTE,” acute coronary syndrome, heart failure and/or cardiogenic shock (main cardiovascular injuries related to COVID-19) compared to healthy controls. The identified genes were further examined in the publicly available transcriptomic dataset for cell/tissue specificity in lung tissue, in different ethnicities and in SARS-CoV-2 infected vs. mock-infected lung tissues and cardiomyocytes.Results: We identified 36 DEGs in blood and endothelium known to play key roles in endothelium and vascular biology, regulation of cellular response to stress as well as endothelial cell migration. Some of these genes were upregulated significantly in SARS-CoV-2 infected lung tissues. On the other hand, some genes with cardioprotective functions were downregulated in SARS-CoV-2 infected cardiomyocytes.Conclusion: In conclusion, our findings from the analysis of publicly available transcriptomic datasets identified shared core genes pertinent to cardiac and vascular-related injuries and their probable role in genetic susceptibility to cardiovascular injury in patients with COVID-19.

Highlights

  • Coronavirus disease 2019 (COVID-19) is a viral respiratory illness caused by the novel coronavirus SARS-CoV-2

  • In light of the premise for a potential role for genetic susceptibility to cardiovascular injuries associated with COVID-19, we further explored for the expression of the identified DEGs in the publicly available dataset (GSE17078) of blood outgrowth endothelial cells from 27 healthy subjects of diverse ages and grouped into Caucasian and African Americans

  • We speculated that if we found common differentially expressed genes shared between the two cell types and which could be affected by SARS-CoV-2 infection, we may be able further to understand the link between COVID-19 and associated endothelium injuries

Read more

Summary

Introduction

Coronavirus disease 2019 (COVID-19) is a viral respiratory illness caused by the novel coronavirus SARS-CoV-2. Patients with pre-existing cardiac disease, hypertension, diabetes, and obesity are more likely to have a severe clinical course with a higher risk of mortality [5,6,7]. There is increasing evidence that a significant number of patients with COVID-19 have cardiovascular involvement, which further increases the likelihood of mortality [5, 6, 8, 9]. The presence of the pre-existing cardiac disease is associated with an increased likelihood of severe clinical course and mortality in patients with COVID-19. Current evidence indicates that a significant number of patients with COVID-19 exhibit cardiovascular involvement even in the absence of known cardiac risk factors. There is a need to understand the underlying mechanisms and genetic predispositions that explain cardiovascular involvement in COVID-19

Objectives
Methods
Results
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.