ArticleAging cell2024
Viral uptake and pathophysiology of the lung endothelial cells in age-associated severe SARS-CoV-2 infection models.
Article in Aging cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Virus-induced endothelial senescence as a cause and driving factor for ME/CFS and long COVID: mediated by a dysfunctional immune system.Cell death & disease · 2026Review
- CT-based phenotyping of COVID-19: cluster analysis of pulmonary and extrapulmonary imaging markers from a multicentre retrospective cohort study.Scientific reports · 2025Article
- Revisiting the monocrotaline-treated rat as a model of inflammatory lung disease: COVID-19 and future pandemic threats?Animal models and experimental medicine · 2025Review
- SARS-CoV-2 uptake and inflammatory response in senescent endothelial cells are regulated by the BSG/VEGFR2 pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- CXCL10-dependent epithelial-vascular cross-talk for endothelial activation following SARS-CoV-2 infection.Scientific reports · 2025Article
- SARS-CoV-2 infection promotes lung thrombosis by inducing integrinβ3 expression in vascular endothelial cells.Scientific reports · 2025Article
- Cytosolic nucleic acid sensing as driver of critical illness: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2025Review
- Proteomic analysis of lung responses to SARS-CoV-2 infection in aged non-human primates: clinical and research relevance.GeroScience · 2024Article
- Spectrum of COVID-19 induced liver injury: A review report.World journal of hepatology · 2024Review
- Viral uptake and pathophysiology of the lung endothelial cells in age-associated severe SARS-CoV-2 infection models.Aging cell · 2024Article
Corrections and comments
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Authors and funding
23 authors at 4 institutions in 1 country.
Funding
Abstract
Thrombosis is the major cause of death in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and the pathology of vascular endothelial cells (ECs) has received much attention. Although there is evidence of the infection of ECs in human autopsy tissues, their detailed pathophysiology remains unclear due to the lack of animal model to study it. We used a mouse-adapted SARS-CoV-2 virus strain in young and mid-aged mice. Only mid-aged mice developed fatal pneumonia with thrombosis. Pulmonary ECs were isolated from these infected mice and RNA-Seq was performed. The pulmonary EC transcriptome revealed that significantly higher levels of viral genes were detected in ECs from mid-aged mice with upregulation of viral response genes such as DDX58 and IRF7. In addition, the thrombogenesis-related genes encoding PLAT, PF4, F3 PAI-1, and P-selectin were upregulated. In addition, the inflammation-related molecules such as CXCL2 and CXCL10 were upregulated in the mid-aged ECs upon viral infection. Our mouse model demonstrated that SARS-CoV-2 virus entry into aged vascular ECs upregulated thrombogenesis and inflammation-related genes and led to fatal pneumonia with thrombosis. Current results of EC transcriptome showed that EC uptake virus and become thrombogenic by activating neutrophils and platelets in the aged mice, suggesting age-associated EC response as a novel finding in human severe COVID-19.
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Registered trials
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