Evidence map›Paper›PMID 35509442›Full record

ArticleERJ open research2022

Heparan sulfate mimetic fucoidan restores the endothelial glycocalyx and protects against dysfunction induced by serum of COVID-19 patients in the intensive care unit.

Lushun Yuan, Shuzhen Cheng, Wendy M P J Sol, Anouk I M van der Velden, Hans Vink, Ton J Rabelink, Bernard M van den Berg

Open access · goldAbstract read
In one paragraph

Article in ERJ open research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
5.6field-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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Endotheliopathy in Acute COVID-19 and Long COVID.International journal of molecular sciences · 2023
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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

7 authors at 2 institutions in 1 country.

Lushun YuanThe Einthoven Laboratory for Vascular and Regenerative Medicine, Dept of Internal Medicine, Nephrology, Leiden University Medical Center, Leiden, The Netherlands.
Shuzhen ChengDept of Internal Medicine, Thrombosis and Hemostasis, Leiden University Medical Center, Leiden, The Netherlands.
Wendy M P J SolThe Einthoven Laboratory for Vascular and Regenerative Medicine, Dept of Internal Medicine, Nephrology, Leiden University Medical Center, Leiden, The Netherlands.
Anouk I M van der VeldenThe Einthoven Laboratory for Vascular and Regenerative Medicine, Dept of Internal Medicine, Nephrology, Leiden University Medical Center, Leiden, The Netherlands.
Hans VinkDept of Physiology, Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands.
Ton J RabelinkThe Einthoven Laboratory for Vascular and Regenerative Medicine, Dept of Internal Medicine, Nephrology, Leiden University Medical Center, Leiden, The Netherlands.
Bernard M van den BergThe Einthoven Laboratory for Vascular and Regenerative Medicine, Dept of Internal Medicine, Nephrology, Leiden University Medical Center, Leiden, The Netherlands.ORCID https://orcid.org/0000-0002-5726-5777
Leiden University Medical Center · NLMaastricht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence proves that endothelial dysfunction is involved in coronavirus disease 2019 (COVID-19) progression. We previously demonstrated that the endothelial surface glycocalyx has a critical role in maintenance of vascular integrity. Here, we hypothesised that serum factors of severe COVID-19 patients affect the glycocalyx and result in endothelial dysfunction. We included blood samples of 32 COVID-19 hospitalised patients at the Leiden University Medical Center, of which 26 were hospitalised in an intensive care unit (ICU) and six on a non-ICU hospital floor; 18 of the samples were obtained from convalescent patients 6 weeks after hospital discharge, and 12 from age-matched healthy donors (control) during the first period of the outbreak. First, we determined endothelial (angiopoietin 2 (ANG2)) and glycocalyx degradation (soluble thrombomodulin (sTM) and syndecan-1 (sSDC1)) markers in plasma. In the plasma of COVID-19 patients, circulating ANG2 and sTM were elevated in patients in the ICU. Primary lung microvascular endothelial cell (HPMEC) and human glomerular microvascular endothelial cell (GEnC) cultured in the presence of these sera led to endothelial cell glycocalyx degradation, barrier disruption, inflammation and increased coagulation on the endothelial surface, significantly different compared to healthy control and non-ICU patient sera. These changes could all be restored in the presence of fucoidan. In conclusion, our data highlight the link between endothelial glycocalyx degradation, barrier failure and induction of a procoagulant surface in COVID-19 patients in ICU which could be targeted earlier in disease by the presence of heparan sulfate mimetics.

Identifiers

PMID35509442
PMCPMC8958944
OpenAlexW4221132096

What OpenQuestion holds

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LicenceCC BY-NC
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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.