Evidence map›Paper›PMID 33781826›Full record

ArticleLife sciences2021

Heparin prevents in vitro glycocalyx shedding induced by plasma from COVID-19 patients.

Simone R Potje, Tiago J Costa, Thais F C Fraga-Silva, Ronaldo B Martins, Maira N Benatti, Carlos E L Almado, Keyla S G de Sá, Vânia L D Bonato, Eurico Arruda, Paulo Louzada-Junior and 5 more

Open access · greenAbstract read
In one paragraph

Article in Life sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 2 pooled it
4.0field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 2 syntheses or guidelines pooled it, 68 citations in OpenAlex.

  1. Endotheliopathy in Acute COVID-19 and Long COVID.International journal of molecular sciences · 2023
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  11. Thromboembolic Events in the Era of COVID-19: A Detailed Narrative Review.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2025
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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

15 authors at 1 institution in 1 country.

Simone R PotjeDepartment of Chemistry and Physics, Faculty of Pharmaceutical Sciences of Ribeirao Preto, University of São Paulo - USP, Brazil; Department of Pharmacology, Ribeirao Preto Medical School, University of São Paulo - USP, Brazil.
Tiago J CostaDepartment of Pharmacology, Ribeirao Preto Medical School, University of São Paulo - USP, Brazil.
Thais F C Fraga-SilvaDepartment of Biochemistry and Immunology, Ribeirao Preto Medical School, University of São Paulo - USP, Brazil.
Ronaldo B MartinsDepartment of Cell and Molecular Biology, Ribeirao Preto Medical School, University of São Paulo - USP, Brazil.
Maira N BenattiDepartment of Clinical Medicine, Division of Internal Medicine, Ribeirao Preto Medical School, University of São Paulo - USP, Brazil.
Carlos E L AlmadoDepartment of Surgery and Anatomy, Division of Intensive Care, Ribeirao Preto Medical School, University of São Paulo - USP, Brazil.
Keyla S G de SáDepartment of Cell and Molecular Biology, Ribeirao Preto Medical School, University of São Paulo - USP, Brazil.
Vânia L D BonatoDepartment of Biochemistry and Immunology, Ribeirao Preto Medical School, University of São Paulo - USP, Brazil.
Eurico ArrudaDepartment of Cell and Molecular Biology, Ribeirao Preto Medical School, University of São Paulo - USP, Brazil.
Paulo Louzada-JuniorDepartment of Clinical Medicine, Division of Internal Medicine, Ribeirao Preto Medical School, University of São Paulo - USP, Brazil.
Rene D R OliveiraDepartment of Clinical Medicine, Division of Internal Medicine, Ribeirao Preto Medical School, University of São Paulo - USP, Brazil.
Dario S ZamboniDepartment of Cell and Molecular Biology, Ribeirao Preto Medical School, University of São Paulo - USP, Brazil.
Christiane BecariDepartment of Surgery and Anatomy, Division of Intensive Care, Ribeirao Preto Medical School, University of São Paulo - USP, Brazil.
Maria Auxiliadora-MartinsDepartment of Surgery and Anatomy, Division of Intensive Care, Ribeirao Preto Medical School, University of São Paulo - USP, Brazil.
Rita C TostesDepartment of Pharmacology, Ribeirao Preto Medical School, University of São Paulo - USP, Brazil. Electronic address: rtostes@usp.br.
Universidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The severe forms and worsened outcomes of COVID-19 (coronavirus disease 19) are closely associated with hypertension and cardiovascular disease. Endothelial cells express Angiotensin-Converting Enzyme 2 (ACE2), which is the entrance door for the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The hallmarks of severe illness caused by SARS-CoV-2 infection are increased levels of IL-6, C-reactive protein, D-dimer, ferritin, neutrophilia and lymphopenia, pulmonary intravascular coagulopathy and microthrombi of alveolar capillaries. The endothelial glycocalyx, a proteoglycan- and glycoprotein-rich layer covering the luminal side of endothelial cells, contributes to vascular homeostasis. It regulates vascular tonus and permeability, prevents thrombosis, and modulates leukocyte adhesion and inflammatory response. We hypothesized that cytokine production and reactive oxygen species (ROS) generation associated with COVID-19 leads to glycocalyx degradation. A cohort of 20 hospitalized patients with a confirmed COVID-19 diagnosis and healthy subjects were enrolled in this study. Mechanisms associated with glycocalyx degradation in COVID-19 were investigated. Increased plasma concentrations of IL-6 and IL1-β, as well as increased lipid peroxidation and glycocalyx components were detected in plasma from COVID-19 patients compared to plasma from healthy subjects. Plasma from COVID-19 patients induced glycocalyx shedding in cultured human umbilical vein endothelial cells (HUVECs) and disrupted redox balance. Treatment of HUVECs with low molecular weight heparin inhibited the glycocalyx perturbation. In conclusion, plasma from COVID-19 patients promotes glycocalyx shedding and redox imbalance in endothelial cells, and heparin treatment potentially inhibits glycocalyx disruption.

Indexed as

AgedBlood Coagulation DisordersCase-Control StudiesCell AdhesionCOVID-19COVID-19 TestingEndothelium, VascularFemaleGlycocalyxHeparinHumansHuman Umbilical Vein Endothelial CellsInterleukin-1betaInterleukin-6MaleMiddle AgedHeparinIL6 protein, humanInterleukin-1betaInterleukin-6COVID-19Endothelial cellsGlycocalyxHeparan sulfate proteoglycansLow molecular weight heparinVascular dysfunction

Identifiers

PMID33781826
PMCPMC7997864
OpenAlexW3145440008

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.