Evidence map›Paper›PMID 33824483›Full record

ReviewNature reviews. Immunology2021

Endothelial dysfunction and immunothrombosis as key pathogenic mechanisms in COVID-19.

Aldo Bonaventura, Alessandra Vecchié, Lorenzo Dagna, Kimberly Martinod, Dave L Dixon, Benjamin W Van Tassell, Francesco Dentali, Fabrizio Montecucco, Steffen Massberg, Marcel Levi and 1 more

Open access · bronzeAbstract readReview
In one paragraph

Review in Nature reviews. Immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 616 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
616citing papers in PubMed, 4 pooled it
52.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

616 citing papers in PubMed, 4 syntheses or guidelines pooled it, 942 citations in OpenAlex.

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  18. Ninjurin2 Promotes Pulmonary Endothelial Barrier Dysfunction Through VEGF/VEGFR2 Signaling Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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556 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 7 institutions in 5 countries.

Aldo BonaventuraPauley Heart Center, Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA. aldo.bonaventura@asst-settelaghi.it.ORCID http://orcid.org/0000-0002-4747-5535
Alessandra VecchiéPauley Heart Center, Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Lorenzo DagnaUnit of Immunology, Rheumatology, Allergy and Rare Diseases, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Kimberly MartinodCenter for Molecular and Vascular Biology, Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium.ORCID http://orcid.org/0000-0002-1026-6107
Dave L DixonPauley Heart Center, Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Benjamin W Van TassellPauley Heart Center, Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Francesco DentaliDepartment of Medicine and Surgery, Insubria University, Varese, Italy.
Fabrizio MontecuccoIRCCS Ospedale Policlinico San Martino Genova - Italian Cardiovascular Network, Genoa, Italy.ORCID http://orcid.org/0000-0003-0823-8729
Steffen MassbergDeutsches Zentrum für Herz-Kreislauf-Forschung (DZHK) e.V., Partner Site Munich Heart Alliance, Munich, Germany.ORCID http://orcid.org/0000-0001-7387-3986
Marcel LeviDepartment of Medicine and Cardio-metabolic Programme - NIHR UCLH/UCL BRC, University College London Hospitals NHS Foundation Trust, London, UK.
Antonio AbbatePauley Heart Center, Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Virginia Commonwealth University · USKU Leuven · BELMU Klinikum · DEOspedale Policlinico San Martino · ITUniversity College London Hospitals NHS Foundation Trust · GBUniversity of Insubria · ITVita-Salute San Raffaele University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronavirus disease 2019 (COVID-19) is a clinical syndrome caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with severe disease show hyperactivation of the immune system, which can affect multiple organs besides the lungs. Here, we propose that SARS-CoV-2 infection induces a process known as immunothrombosis, in which activated neutrophils and monocytes interact with platelets and the coagulation cascade, leading to intravascular clot formation in small and larger vessels. Microthrombotic complications may contribute to acute respiratory distress syndrome (ARDS) and other organ dysfunctions. Therapeutic strategies aimed at reducing immunothrombosis may therefore be useful. Several antithrombotic and immunomodulating drugs have been proposed as candidates to treat patients with SARS-CoV-2 infection. The growing understanding of SARS-CoV-2 infection pathogenesis and how it contributes to critical illness and its complications may help to improve risk stratification and develop targeted therapies to reduce the acute and long-term consequences of this disease.

Indexed as

Blood CoagulationBlood PlateletsCOVID-19Critical IllnessCytokine Release SyndromeEndothelium, VascularFibrinolytic AgentsHumansImmunity, InnateLungMonocytesNeutrophilsSARS-CoV-2Venous ThrombosisFibrinolytic Agents

Identifiers

PMID33824483
PMCPMC8023349
OpenAlexW3140915421

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.