Evidence map›Paper›PMID 29880486›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2018

Endothelial Glycocalyx as a Shield Against Diabetic Vascular Complications: Involvement of Hyaluronan and Hyaluronidases.

Sophie Dogné, Bruno Flamion, Nathalie Caron

Open access · bronzeAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
12.1field-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

96 citing papers in PubMed, 1 synthesis or guideline pooled it, 165 citations in OpenAlex.

  1. Pooled it
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  6. Endothelial Exostosin-1 Is Needed for Glycocalyx Integrity and Inflammatory Resolution in Acute Lung Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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36 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

3 authors at 1 institution in 1 country.

Sophie DognéFrom the Molecular Physiology Research Unit-URPhyM, Namur Research Institute for Life Sciences (NARILIS), University of Namur (Unamur), Belgium. sophie.dogne@unamur.be.
Bruno FlamionFrom the Molecular Physiology Research Unit-URPhyM, Namur Research Institute for Life Sciences (NARILIS), University of Namur (Unamur), Belgium.
Nathalie CaronFrom the Molecular Physiology Research Unit-URPhyM, Namur Research Institute for Life Sciences (NARILIS), University of Namur (Unamur), Belgium.
University of Namur · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The endothelial glycocalyx (EG), which covers the apical surface of the endothelial cells and floats into the lumen of the vessels, is a key player in vascular integrity and cardiovascular homeostasis. The EG is composed of PGs (proteoglycans), glycoproteins, glycolipids, and glycosaminoglycans, in particular hyaluronan (HA). HA seems to be implicated in most of the functions described for EG such as creating a space between blood and the endothelium, controlling vessel permeability, restricting leukocyte and platelet adhesion, and allowing an appropriate endothelial response to flow variation through mechanosensing. The amount of HA in the EG may be regulated by HYAL (hyaluronidase) 1, the most active somatic hyaluronidase. HYAL1 seems enriched in endothelial cells through endocytosis from the bloodstream. The role of the other main somatic hyaluronidase, HYAL2, in the EG is uncertain. Damage to the EG, accompanied by shedding of one or more of its components, is an early sign of various pathologies including diabetes mellitus. Shedding increases the blood or plasma concentration of several EG components, such as HA, heparan sulfate, and syndecan. The plasma levels of these molecules can then be used as sensitive markers of EG degradation. This has been shown in type 1 and type 2 diabetic patients. Recent experimental studies suggest that preserving the size and amount of EG HA in the face of diabetic insults could be a useful novel therapeutic strategy to slow diabetic complications. One way to achieve this goal, as suggested by a murine model of HYAL1 deficiency, may be to inhibit the function of HYAL1. The same approach may succeed in other pathological situations involving endothelial dysfunction and EG damage.

Indexed as

AnimalsDiabetes MellitusDiabetic AngiopathiesEndothelial CellsEndothelium, VascularEnzyme InhibitorsGlycocalyxHumansHyaluronic AcidHyaluronoglucosaminidaseMechanotransduction, CellularEnzyme InhibitorsHYAL1 protein, humanHyal1 protein, mouseHyaluronic AcidHyaluronoglucosaminidasecardiovascular diseasediabetes mellitusendothelial cellsglycocalyxhyaluronic acidpermeability

Identifiers

PMID29880486
PMCPMC6039403
OpenAlexW2980718418

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.