Evidence map›Paper›PMID 33032965›Full record

ReviewBiomedical journal2020

Endothelial glycocalyx damage as a systemic inflammatory microvascular endotheliopathy in COVID-19.

Minako Yamaoka-Tojo

Open access · goldAbstract readReview
In one paragraph

Review in Biomedical journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 8% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Endotheliopathy in Acute COVID-19 and Long COVID.International journal of molecular sciences · 2023
    Pooled it
  2. Trial
  3. Review
  4. Observational
  5. Review
  6. Article
  7. Post-COVID-19 Jaw Osteonecrosis: A Narrative Review.Medicina (Kaunas, Lithuania) · 2026
    Review
  8. Article
  9. Observational
  10. Article
  11. Article
  12. Review
  13. Observational
  14. Single-cell RNA sequencing: new insights for pulmonary endothelial cells.Frontiers in cell and developmental biology · 2025
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Minako Yamaoka-TojoDepartment of Rehabilitation/Regenerative Medicine and Cell Design Research Facility, Kitasato University School of Allied Health Sciences, Sagamihara, Japan; Department of Cardiovascular Medicine, Kitasato University Graduate School of Medical Sciences, Sagamihara, Japan. Electronic address: myamaoka@med.kitasato-u.ac.jp.
Kitasato University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In atherosclerosis patients, vascular endothelial dysfunction is commonly observed alongside damage of the vascular endothelial glycocalyx, an extracellular matrix bound to and encapsulating the endothelial cells lining the blood vessel wall. Although atherosclerotic risk factors have been reported in severe patients with coronavirus disease 2019 (COVID-19), the exact mechanisms are unclear. The mortality associated with the COVID-19 outbreak is increased by comorbidities, including hypertension, diabetes, obesity, chronic obstructive pulmonary disease (COPD), and cardiovascular disease. Besides, older individuals and smokers have significantly worse outcomes. Interestingly, these comorbidities and risk factors are consistent with the pathophysiology that causes vascular endothelial glycocalyx damage. Moreover, vascular glycocalyx dysfunction causes microvascular leakage, which results in interstitial pulmonary abnormal shadows (multiple patchy shadows with a ground glass inter-pneumonic appearance). This is frequently followed by severe acute respiratory distress syndrome (ARDS), closely related to coagulo-fibrinolytic changes contributing to disseminated intravascular coagulation (DIC) and Kawasaki disease shock syndrome, as well as inducing activation of the coagulation cascade, leading to thromboembolism and multiple organ failure. Notably, SARS-CoV-2, the causative virus of COVID-19, binds to ACE2, which is abundantly present not only in human epithelia of the lung and the small intestine, but also in vascular endothelial cells and arterial smooth muscle cells. Moreover, COVID-19 can induce severe septic shock, and sepsis can easily lead to systemic degradation of the vascular endothelial glycocalyx. In the current review, we propose new concepts and therapeutic goals for COVID-19-related vascular endothelial glycocalyx damage, based on previous vascular endothelial medicine research.

Indexed as

COVID-19Endothelial CellsGlycocalyxHumansLungRespiratory Distress SyndromeSARS-CoV-2ARDSCytokine stormKawasaki disease shock syndromeSystemic inflammatory responseVascular endothelial dysfunction

Identifiers

PMID33032965
PMCPMC7443638
OpenAlexW3080822893

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.