ArticleScientific reports2021
Endothelial glycocalyx shields the interaction of SARS-CoV-2 spike protein with ACE2 receptors.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 55 citations in OpenAlex.
- Cardiovascular burden of long coronavirus disease: Clinical challenges and emerging biomarkers.World journal of cardiology · 2026Review
- Glycocalyx at the host-virus interface: a double-edged sword in virus infection and tissue damage.Frontiers in molecular biosciences · 2026Review
- Febrile temperature enhancesbioRxiv : the preprint server for biology · 2025Article
- Glycocalyx Disintegration Is Associated with Mortality in Chronic Heart Failure.Journal of clinical medicine · 2025Article
- Cardiovascular damage and comorbidities related to long COVID: pathomechanisms, prevention, and therapy.Frontiers in cardiovascular medicine · 2025Review
- The Glycocalyx: The Importance of Sugar Coating the Blood-Brain Barrier.International journal of molecular sciences · 2024Review
- Protecting the endothelial glycocalyx in COVID-19.PLoS pathogens · 2024Article
- The Multisystem Impact of Long COVID: A Comprehensive Review.Diagnostics (Basel, Switzerland) · 2024Review
- Review
- Absence of a causal link between COVID-19 and deep vein thrombosis: Insights from a bi-directional Mendelian randomisation study.Journal of global health · 2024Article
- Neurovascular coupling impairment as a mechanism for cognitive deficits in COVID-19.Brain communications · 2024Review
- Reactive oxygen species in endothelial signaling in COVID-19: Protective role of the novel peptide PIP-2.PloS one · 2024Article
- Unraveling the SARS-CoV-2 spike protein long-term effect on neuro-PASC.Frontiers in cellular neuroscience · 2024Article
- Vascular Dysfunctions Contribute to the Long-Term Cognitive Deficits Following COVID-19.Biology · 2023Review
- Observational
- Risk of Thrombosis during and after a SARS-CoV-2 Infection: Pathogenesis, Diagnostic Approach, and Management.Hematology reports · 2023Review
- Endothelial dysfunction in COVID-19: an overview of evidence, biomarkers, mechanisms and potential therapies.Acta pharmacologica Sinica · 2023Review
- Microvascular Thrombosis as a Critical Factor in Severe COVID-19.International journal of molecular sciences · 2023Article
- Severe COVID-19-A Review of Suggested Mechanisms Based on the Role of Extracellular Matrix Stiffness.International journal of molecular sciences · 2023Review
- Potential long-term effects of SARS-CoV-2 infection on the pulmonary vasculature: Multilayered cross-talks in the setting of coinfections and comorbidities.PLoS pathogens · 2023Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Endothelial cells (ECs) play a crucial role in the development and propagation of the severe COVID-19 stage as well as multiorgan dysfunction. It remains, however, controversial whether COVID-19-induced endothelial injury is caused directly by the infection of ECs with SARS-CoV-2 or via indirect mechanisms. One of the major concerns is raised by the contradictory data supporting or denying the presence of ACE2, the SARS-CoV-2 binding receptor, on the EC surface. Here, we show that primary human pulmonary artery ECs possess ACE2 capable of interaction with the viral Spike protein (S-protein) and demonstrate the crucial role of the endothelial glycocalyx in the regulation of the S-protein binding to ACE2 on ECs. Using force spectroscopy method, we directly measured ACE2- and glycocalyx-dependent adhesive forces between S-protein and ECs and characterized the nanomechanical parameters of the cells exposed to S-protein. We revealed that the intact glycocalyx strongly binds S-protein but screens its interaction with ACE2. Reduction of glycocalyx layer exposes ACE2 receptors and promotes their interaction with S-protein. These results indicate that the susceptibility of ECs to COVID-19 infection may depend on the glycocalyx condition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.