ArticleScientific reports2022
Senescent endothelial cells are predisposed to SARS-CoV-2 infection and subsequent endothelial dysfunction.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 38 citations in OpenAlex.
- Beneficial effects of L-Arginine in patients hospitalized for COVID-19: New insights from a randomized clinical trial.Pharmacological research · 2023Trial
- Exploring molecular signatures of senescence with marker, an R Toolkit for evaluating gene sets as phenotypic markers.NAR genomics and bioinformatics · 2026Article
- Senolytic Treatment Reduces Acute and Chronic Lung Inflammation in an Aged Mouse Model of Influenza.Aging cell · 2026Article
- 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
- Longitudinal trajectories of hematological indices and serum metalloproteinases-2 and 9 over 1 year after moderate and severe COVID-19.Frontiers in medicine · 2026Article
- Replicative and stress-induced premature senescence distinctively affect the endothelial anticoagulation capacity.PloS one · 2026Article
- SARS-CoV-2 enhances complement-mediated endothelial injury via the suppression of membrane complement regulatory proteins.Emerging microbes & infections · 2025Article
- 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
- A transcriptome-based human universal senescence index (hUSI) robustly predicts cellular senescence under various conditions.Nature aging · 2025Article
- The Molecular Mechanisms of Cognitive Dysfunction in Long COVID: A Narrative Review.International journal of molecular sciences · 2025Review
- Impact of SARS-CoV-2 Wuhan and Omicron Variant Proteins on Type I Interferon Response.Viruses · 2025Article
- Endothelial growth media components alter SARS-CoV-2 spike-directed growth kinetics.Journal of virological methods · 2025Article
- Nicotinamide mononucleotide restores impaired metabolism, endothelial cell proliferation and angiogenesis in old sedentary male mice.iScience · 2025Article
- Plasma miR-1-3p levels predict severity in hospitalized COVID-19 patients.British journal of pharmacology · 2025Article
- Natural Products to Promote Vascular Health.Handbook of experimental pharmacology · 2025Review
- SARS-CoV-2 infection of human pluripotent stem cell-derived vascular cells reveals smooth muscle cells as key mediators of vascular pathology during infection.Nature communications · 2024Article
- All eyes on PCS: analysis of the retinal microvasculature in patients with post-COVID syndrome-study protocol of a 1 year prospective case-control study.European archives of psychiatry and clinical neuroscience · 2024Article
- Proteomic analysis of lung responses to SARS-CoV-2 infection in aged non-human primates: clinical and research relevance.GeroScience · 2024Article
- Interactions of SARS-CoV-2 with Human Target Cells-A Metabolic View.International journal of molecular sciences · 2024Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The coronavirus disease 2019 (COVID-19), caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains to spread worldwide. COVID-19 is characterized by the striking high mortality in elderly; however, its mechanistic insights remain unclear. Systemic thrombosis has been highlighted in the pathogenesis of COVID-19, and lung microangiopathy in association with endothelial cells (ECs) injury has been reported by post-mortem analysis of the lungs. Here, we experimentally investigated the SARS-CoV-2 infection in cultured human ECs, and performed a comparative analysis for post-infection molecular events using early passage and replicative senescent ECs. We found that; (1) SARS-CoV-2 infects ECs but does not replicate and disappears in 72 hours without causing severe cell damage, (2) Senescent ECs are highly susceptible to SARS-CoV-2 infection, (3) SARS-CoV-2 infection alters various genes expression, which could cause EC dysfunctions, (4) More genes expression is affected in senescent ECs by SARS-CoV-2 infection than in early passage ECs, which might causes further exacerbated dysfunction in senescent ECs. These data suggest that sustained EC dysfunctions due to SARS-CoV-2 infection may contribute to the microangiopathy in the lungs, leading to deteriorated inflammation and thrombosis in COVID-19. Our data also suggest a possible causative role of EC senescence in the aggravated disease in elder COVID-19 patients.
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