ArticleCardiovascular research2022
Preferential uptake of SARS-CoV-2 by pericytes potentiates vascular damage and permeability in an organoid model of the microvasculature.
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 29 papers.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- Enabling Technologies in Vascular Biology: Microphysiological Systems, Organoids, and Beyond.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Article
- Unveiling alternate pathways for SARS-CoV-2 infection via extracellular vesicle-mediated transfer of ACE2 and TMPRSS2.Nature communications · 2026Article
- Super-resolution ultrasound quantifying microvascular alterations for early detection of metastatic cervical lymph nodes: a prospective diagnostic study.Scientific reports · 2025Article
- Decoding long COVID-associated cardiovascular dysfunction: Mechanisms, models, and new approach methodologies.Journal of molecular and cellular cardiology · 2025Review
- A survey of SARS-CoV-2 tropism.Infectious diseases & immunity · 2025Review
- MULTIFACETED ROLES OF PERICYTES IN LUNG INJURY AND REPAIR.Transactions of the American Clinical and Climatological Association · 2025Review
- Intestinal barrier compromise, viral persistence, and immune dysregulation converge on neurological sequelae in Long COVID.Frontiers in aging neuroscience · 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
- Studying the Pulmonary Endothelium in Health and Disease: An Official American Thoracic Society Workshop Report.American journal of respiratory cell and molecular biology · 2024Article
- Postinfectious Pulmonary Complications: Establishing Research Priorities to Advance the Field: An Official American Thoracic Society Workshop Report.Annals of the American Thoracic Society · 2024Review
- The new era of cardiovascular research: revolutionizing cardiovascular research with 3D models in a dish.Medical review (2021) · 2024Review
- Possible mechanisms of SARS-CoV-2-associated myocardial fibrosis: reflections in the post-pandemic era.Frontiers in microbiology · 2024Review
- COVID-19 shed light on Virchow's law of thrombosis.Autopsy & case reports · 2024Article
- SARS-CoV-2 and vascular dysfunction: a growing role for pericytes.Cardiovascular research · 2023Article
- Development trends of human organoid-based COVID-19 research based on bibliometric analysis.Cell proliferation · 2023Review
- The long-term health outcomes, pathophysiological mechanisms and multidisciplinary management of long COVID.Signal transduction and targeted therapy · 2023Review
- Organoids to Remodel SARS-CoV-2 Research: Updates, Limitations and Perspectives.Aging and disease · 2023Review
- Blood Coagulation and Beyond: Position Paper from the Fourth Maastricht Consensus Conference on Thrombosis.Thrombosis and haemostasis · 2023Article
- Pericyte Loss in Diseases.Cells · 2023Review
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
aimsThrombotic complications and vasculopathy have been extensively associated with severe COVID-19 infection; however, the mechanisms inducing endotheliitis and the disruption of endothelial integrity in the microcirculation are poorly understood. We hypothesized that within the vessel wall, pericytes preferentially take up viral particles and mediate the subsequent loss of vascular integrity. METHODS AND
resultsImmunofluorescence of post-mortem patient sections was used to assess pathophysiological aspects of COVID-19 infection. The effects of COVID-19 on the microvasculature were assessed using a vascular organoid model exposed to live viral particles or recombinant viral antigens. We find increased expression of the viral entry receptor angiotensin-converting enzyme 2 on pericytes when compared to vascular endothelium and a reduction in the expression of the junctional protein CD144, as well as increased cell death, upon treatment with both live virus and/or viral antigens. We observe a dysregulation of genes implicated in vascular permeability, including Notch receptor 3, angiopoietin-2, and TEK. Activation of vascular organoids with interleukin-1β did not have an additive effect on vascular permeability. Spike antigen was detected in some patients' lung pericytes, which was associated with a decrease in CD144 expression and increased platelet recruitment and von Willebrand factor (VWF) deposition in the capillaries of these patients, with thrombi in large vessels rich in VWF and fibrin.
conclusionTogether, our data indicate that direct viral exposure to the microvasculature modelled by organoid infection and viral antigen treatment results in pericyte infection, detachment, damage, and cell death, disrupting pericyte-endothelial cell crosstalk and increasing microvascular endothelial permeability, which can promote thrombotic and bleeding complications in the microcirculation.
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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.