Evidence map›Paper›PMID 34033751›Full record

ReviewThe American journal of pathology2021

COVID-19 Vasculopathy: Mounting Evidence for an Indirect Mechanism of Endothelial Injury.

Roberto F Nicosia, Giovanni Ligresti, Nunzia Caporarello, Shreeram Akilesh, Domenico Ribatti

Open access · bronzeAbstract readReview
In one paragraph

Review in The American journal of pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 3% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Observational
  6. Review
  7. Article
  8. Article
  9. Review
  10. Coronary Implications of COVID-19.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2025
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Vascular Contribution to Lung Repair and Fibrosis.American journal of respiratory cell and molecular biology · 2023
    Review

9 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Roberto F NicosiaDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, Washington. Electronic address: rnicosia@uw.edu.
Giovanni LigrestiDepartment of Medicine, Boston University School of Medicine, Boston, Massachusetts.
Nunzia CaporarelloDepartment of Physiology & Biomedical Engineering, Mayo Clinic, Rochester, Minnesota.
Shreeram AkileshDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, Washington.
Domenico RibattiDepartment of Basic Medical Sciences, Neuroscienze e Organi di Senso (SMBNOS), Universita' degli Studi Aldo Moro, Policlinico, Bari, Italy.
University of Washington · USMayo Clinic · USUniversity of Bari Aldo Moro · IT

Funding

Tissue Chip Data to the Microphysiology Systems Database (MPS-Db) Supplement to A Microphysiological System for Kidney Disease Modeling and Drug Efficacy TestingUH3TR002158 · NCATS · UNIVERSITY OF WASHINGTON · PI HIMMELFARB, JONATHAN · 2019 to 2021
$4.2M
Epigenetic regulation of pulmonary fibrosisR01HL142596 · NHLBI · MAYO CLINIC ROCHESTER · PI Giovanni Ligresti · 2018 to 2026
$2.9M
NCATS NIH HHS UH3 TR002158NHLBI NIH HHS R01 HL142596
6 · The paper itself

Abstract

Patients with coronavirus disease 2019 (COVID-19) who are critically ill develop vascular complications characterized by thrombosis of small, medium, and large vessels. Dysfunction of the vascular endothelium due to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been implicated in the pathogenesis of the COVID-19 vasculopathy. Although initial reports suggested that endothelial injury was caused directly by the virus, recent studies indicate that endothelial cells do not express angiotensin-converting enzyme 2, the receptor that SARS-CoV-2 uses to gain entry into cells, or express it at low levels and are resistant to the infection. These new findings, together with the observation that COVID-19 triggers a cytokine storm capable of injuring the endothelium and disrupting its antithrombogenic properties, favor an indirect mechanism of endothelial injury mediated locally by an augmented inflammatory reaction to infected nonendothelial cells, such as the bronchial and alveolar epithelium, and systemically by the excessive immune response to infection. Herein we review the vascular pathology of COVID-19 and critically discuss the potential mechanisms of endothelial injury in this disease.

Indexed as

Angiotensin-Converting Enzyme 2BronchiCOVID-19Cytokine Release SyndromeEndothelium, VascularHumansPulmonary AlveoliRespiratory MucosaSARS-CoV-2ThrombosisACE2 protein, humanAngiotensin-Converting Enzyme 2

Identifiers

PMID34033751
PMCPMC8141344
OpenAlexW3164721049

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.