Evidence map›Paper›PMID 30988234›Full record

ReviewBiorheology2019

Endothelial barrier reinforcement relies on flow-regulated glycocalyx, a potential therapeutic target.

Ian C Harding, Ronodeep Mitra, Solomon A Mensah, Alina Nersesyan, Nandita N Bal, Eno E Ebong

Open access · greenAbstract readReview
In one paragraph

Review in Biorheology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.5field-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

23 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. TheeLife · 2025
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Endothelial mechanobiology in atherosclerosis.Cardiovascular research · 2023
    Review
  10. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Role of endothelial cells in vascular calcification.Frontiers in cardiovascular medicine · 2022
    Review
  17. Observational
  18. Article
  19. Review
  20. Review
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

6 authors at 2 institutions in 1 country.

Ian C HardingDepartment of Bioengineering, Northeastern University, Boston, MA, USA.
Ronodeep MitraDepartment of Chemical Engineering, Northeastern University, Boston, MA, USA.
Solomon A MensahDepartment of Bioengineering, Northeastern University, Boston, MA, USA.
Alina NersesyanDepartment of Bioengineering, Northeastern University, Boston, MA, USA.
Nandita N BalDepartment of Chemical Engineering, Northeastern University, Boston, MA, USA.
Eno E EbongDepartment of Bioengineering, Northeastern University, Boston, MA, USA.
Northeastern University · USAlbert Einstein College of Medicine · US

Funding

Atheroprotective vs. Atherogenic Glycocalyx Mechanotransduction MechanismsK01HL125499 · NHLBI · NORTHEASTERN UNIVERSITY · PI EBONG, ENO ESSIEN · 2015 to 2019
$770k
NHLBI NIH HHS K01 HL125499
6 · The paper itself

Abstract

backgroundThe onset of many disease processes depends on the function of the endothelial cell (EC) glycocalyx (GCX) which acts as a flow-dependent barrier to cellular infiltration and molecular transport across the blood vessel wall.

objectiveThis review aims to examine these processes with the potential end goal of implementing GCX repair to restore EC barrier function and slow the progression of disease.

methodsCell and mouse studies were employed to examine the state of EC GCX in healthy versus disruptive flow conditions. Correlations of observations of the GCX with a number of EC functions were sought with an emphasis on studies of trans-endothelial barrier integrity against vessel wall infiltration of cells and molecules from the circulation. To demonstrate the importance of GCX as a regulator of trans-endothelial infiltration, assays were performed using ECs with an intact GCX and compared to assays of ECs with an experimentally degraded GCX. Studies were also conducted of ECs in which a degraded GCX was repaired.

resultsIn healthy flow conditions, the EC GCX was found to be thick and substantially covered the endothelial surface. GCX expression dropped significantly in complex flow conditions and coincided with a disease-like cellular and molecular accumulation in the endothelium or within the blood vessel wall. Therapeutic repair of the GCX abolished this accumulation.

conclusionsRegenerating the degraded GCX reverses EC barrier dysfunction and may attenuate the progression of vascular disease.

Indexed as

HemodynamicsAnimalsCapillary PermeabilityEndothelial CellsEndothelium, VascularGlycocalyxHumansMiceVascular Diseasesatherosclerosiscancer metastasisendothelial dysfunctionEndothelial glycocalyxfluid shear stressvascular inflammation

Identifiers

PMID30988234
PMCPMC6766428
OpenAlexW2940383347

What OpenQuestion holds

Textmetadata
LicenceTDM
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.