ArticleCardiovascular research2022
Cardiac SARS-CoV-2 infection is associated with pro-inflammatory transcriptomic alterations within the heart.
Article in Cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 86 citations in OpenAlex.
- Spike 1 protein of SARS-CoV-2 induces endothelial inflammation and vascular dysfunction through interferon ISG15-dependent mechanisms.Cardiovascular research · 2026Article
- Dietary Glycerol Monolaurate Enhances Growth and Immune Function in Calves via Hepatic Immunometabolic Reprogramming.Veterinary sciences · 2026Article
- Unraveling the cardiovascular burden of long COVID: symptom profiles, underlying mechanisms, and clinical management insights.Frontiers in cardiovascular medicine · 2026Review
- Organoids in respiratory virus research: advances and perspectives.Molecular biomedicine · 2025Review
- A survey of SARS-CoV-2 tropism.Infectious diseases & immunity · 2025Review
- Membrane Protein of SARS-CoV-2 Promotes the Production of CXCL10 and Apoptosis of Myocardial Cells.Cardiovascular toxicology · 2025Article
- Viral Infection and Connexin Dysfunction in the Heart.Current cardiology reports · 2025Review
- Review
- Risk impact of SARS-CoV-2 coronavirus and spike protein on cardiac tissue: a comprehensive review.Physiological research · 2024Review
- Cardiac Arrhythmias and Autonomic Dysfunction Associated With COVID-19: A Scientific Statement From the American Heart Association.Circulation · 2024Review
- Infiltrating monocytes drive cardiac dysfunction in a cardiomyocyte-restricted mouse model of SARS-CoV-2 infection.Journal of virology · 2024Article
- Interactions of SARS-CoV-2 with Human Target Cells-A Metabolic View.International journal of molecular sciences · 2024Review
- SARS-CoV-2 variants divergently infect and damage cardiomyocytes in vitro and in vivo.Cell & bioscience · 2024Article
- Evaluation of blood pressure variation in recovered COVID-19 patients at one-year follow-up: a retrospective cohort study.BMC cardiovascular disorders · 2024Article
- The emerging role of heart-on-a-chip systems in delineating mechanisms of SARS-CoV-2-induced cardiac dysfunction.Bioengineering & translational medicine · 2024Review
- Differential analysis of IBV-infected primary chicken embryonic fibroblasts and immortalized DF-1.Microbiology spectrum · 2024Article
- Interferons and interferon-related pathways in heart disease.Frontiers in cardiovascular medicine · 2024Review
- GPR15-mediated T cell recruitment during acute viral myocarditis facilitated virus elimination and improved outcome.Nature cardiovascular research · 2024Article
- UnravelingFrontiers in oncology · 2024Review
- Transcriptome and machine learning analysis of the impact of COVID-19 on mitochondria and multiorgan damage.PloS one · 2024Article
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Authors and funding
23 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsCardiac involvement in COVID-19 is associated with adverse outcome. However, it is unclear whether cell-specific consequences are associated with cardiac SARS-CoV-2 infection. Therefore, we investigated heart tissue utilizing in situ hybridization, immunohistochemistry, and RNA-sequencing in consecutive autopsy cases to quantify virus load and characterize cardiac involvement in COVID-19. METHODS AND
resultsIn this study, 95 SARS-CoV-2-positive autopsy cases were included. A relevant SARS-CoV-2 virus load in the cardiac tissue was detected in 41/95 deceased (43%). Massive analysis of cDNA ends (MACE)-RNA-sequencing was performed to identify molecular pathomechanisms caused by the infection of the heart. A signature matrix was generated based on the single-cell dataset 'Heart Cell Atlas' and used for digital cytometry on the MACE-RNA-sequencing data. Thus, immune cell fractions were estimated and revealed no difference in immune cell numbers in cases with and without cardiac infection. This result was confirmed by quantitative immunohistological diagnosis. MACE-RNA-sequencing revealed 19 differentially expressed genes (DEGs) with a q-value <0.05 (e.g. up: IFI44L, IFT3, TRIM25; down: NPPB, MB, MYPN). The upregulated DEGs were linked to interferon pathways and originate predominantly from endothelial cells. In contrast, the downregulated DEGs originate predominately from cardiomyocytes. Immunofluorescent staining showed viral protein in cells positive for the endothelial marker ICAM1 but rarely in cardiomyocytes. The Gene Ontology (GO) term analysis revealed that downregulated GO terms were linked to cardiomyocyte structure, whereas upregulated GO terms were linked to anti-virus immune response.
conclusionThis study reveals that cardiac infection induced transcriptomic alterations mainly linked to immune response and destruction of cardiomyocytes. While endothelial cells are primarily targeted by the virus, we suggest cardiomyocyte destruction by paracrine effects. Increased pro-inflammatory gene expression was detected in SARS-CoV-2-infected cardiac tissue but no increased SARS-CoV-2 associated immune cell infiltration was observed.
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