ArticleOpen biology2020
Vascular underpinning of COVID-19.
Article in Open biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Risk factors for severe COVID-19 disease increase SARS-CoV-2 infectivity of endothelial cells and pericytes.Open biology · 2024Article
- Is COVID-19 Infection a Multiorganic Disease? Focus on Extrapulmonary Involvement of SARS-CoV-2.Journal of clinical medicine · 2024Review
- Complement factor D targeting protects endotheliopathy in organoid and monkey models of COVID-19.Cell stem cell · 2023Article
- Molecular Analysis of SARS-CoV-2 Spike Protein-Induced Endothelial Cell Permeability and vWF Secretion.International journal of molecular sciences · 2023Article
- Article
- Anti-COVID-19 potential ofScientific African · 2022Review
- Effects of SARS CoV-2, COVID-19, and its vaccines on male sexual health and reproduction: where do we stand?International journal of impotence research · 2022Review
- SARS-CoV-2, platelets, and endothelium: coexistence in space and time, or a pernicious ménage à trois?Vascular biology (Bristol, England) · 2022Review
- Endothelial cells and blood vessels are major targets for COVID-19-induced tissue injury and spreading to various organs.World journal of gastroenterology · 2022Article
- Prognostic value of HAmerican heart journal plus : cardiology research and practice · 2022Article
- Persistent Lung Injury and Prothrombotic State in Long COVID.Frontiers in immunology · 2022Review
- Article
- The pathogenic role of epithelial and endothelial cells in early-phase COVID-19 pneumonia: victims and partners in crime.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021Review
- Problems of Pathogenesis and Pathogenetic Therapy of COVID-19 from the Perspective of the General Theory of Pathological Systems (General Pathological Processes).International journal of molecular sciences · 2021Review
- 8806 Russian patients demonstrate T cell count as better marker of COVID-19 clinical course severity than SARS-CoV-2 viral load.Scientific reports · 2021Article
- Endothelial Cells in Emerging Viral Infections.Frontiers in cardiovascular medicine · 2021Review
- SARS-CoV-2 Infects Endothelial CellsFrontiers in cellular and infection microbiology · 2021Article
- Harnessing biomaterials for therapeutic strategies against COVID-19.Emergent materials · 2021Review
- Mechanisms of SARS-CoV-2-induced lung vascular disease: potential role of complement.Pulmonary circulationReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
COVID-19 management guidelines have largely attributed critically ill patients who develop acute respiratory distress syndrome, to a systemic overproduction of pro-inflammatory cytokines. Cardiovascular dysfunction may also represent a primary phenomenon, with increasing data suggesting that severe COVID-19 reflects a confluence of vascular dysfunction, thrombosis and dysregulated inflammation. Here, we first consolidate the information on localized microvascular inflammation and disordered cytokine release, triggering vessel permeability and prothrombotic conditions that play a central role in perpetuating the pathogenic COVID-19 cascade. Secondly, we seek to clarify the gateways which SARS-CoV-2, the causative COVID-19 virus, uses to enter host vascular cells. Post-mortem examinations of patients' tissues have confirmed direct viral endothelial infection within several organs. While there have been advances in single-cell RNA sequencing, endothelial cells across various vascular beds express low or undetectable levels of those touted SARS-CoV-2 entry factors. Emerging studies postulate alternative pathways and the apicobasal distribution of host cell surface factors could influence endothelial SARS-CoV-2 entry and replication. Finally, we provide experimental considerations such as endothelial polarity, cellular heterogeneity in organoids and shear stress dynamics in designing cellular models to facilitate research on viral-induced endothelial dysfunctions. Understanding the vascular underpinning of COVID-19 pathogenesis is crucial to managing outcomes and mortality.
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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.