Evidence map›Paper›PMID 29127504›Full record

ReviewCurrent atherosclerosis reports2017

Glycocalyx in Atherosclerosis-Relevant Endothelium Function and as a Therapeutic Target.

Ronodeep Mitra, Gerard Leland O'Neil, Ian Chandler Harding, Ming Jie Cheng, Solomon Arko Mensah, Eno Essien Ebong

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Current atherosclerosis reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
8.1field-weighted citation impact, top 2% 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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Observational
  5. Article
  6. Observational
  7. Review
  8. Manuscript DMD-D-25-00346 The impact of glycocalyx on partitioning and distribution of basic drugs.Drug metabolism and disposition: the biological fate of chemicals · 2026
    Article
  9. Article
  10. Vascular Mechanobiology: From Membrane to Nucleus.Advances in experimental medicine and biology · 2026
    Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Observational
  18. Article
  19. Review
  20. Review

14 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

6 authors at 1 institution in 1 country.

Ronodeep MitraDepartment of Bioengineering, Northeastern University, Boston, MA, USA.
Gerard Leland O'NeilDepartment of Biology, Northeastern University, Boston, MA, USA.
Ian Chandler HardingDepartment of Bioengineering, Northeastern University, Boston, MA, USA.
Ming Jie ChengDepartment of Chemical Engineering, Northeastern University, 360 Huntington Avenue 313 Snell Engineering Building, Boston, MA, 02115, USA.
Solomon Arko MensahDepartment of Bioengineering, Northeastern University, Boston, MA, USA.
Eno Essien EbongDepartment of Bioengineering, Northeastern University, Boston, MA, USA. e.ebong@northeastern.edu.
Northeastern University · 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

purpose of reviewThe cell surface-attached extracellular glycocalyx (GCX) layer is a major contributor to endothelial cell (EC) function and EC-dependent vascular health and is a first line of defense against vascular diseases including atherosclerosis. Here, we highlight our findings regarding three GCX-dependent EC functions, which are altered when GCX is shed and in atherosclerosis. We discuss why the GCX is a viable option for the prevention and treatment of atherosclerosis. RECENT

findingsGCX regulated EC activities such as barrier and filtration function, active cell-to-cell communication, and vascular tone mediation contribute to function of the entire vascular wall. Atheroprone vessel regions, including bifurcation sites, exhibit breakdown in GCX. This GCX degradation allows increased lipid flux and thereby promotes lipid deposition in the vessel walls, a hallmark of atherosclerosis. GCX degradation also alters EC-to-EC communication while increasing EC-to-inflammatory cell interactions that enable inflammatory cells to migrate into the vessel wall. Inflammatory macrophages and foam cells, to be specific, appear in early stages of atherosclerosis. Furthermore, GCX degradation deregulates vascular tone, by causing ECs to reduce their expression of endothelial nitric oxide synthase (eNOS) which produces the vasodilator, nitric oxide. Loss of vasodilation supports vasoconstriction, which promotes the progression of atherosclerosis. Common medicinal atherosclerosis therapies include lipid lowering and anti-platelet therapies. None of these treatments specifically target the endothelial GCX, although the GCX is at the front-line in atherosclerosis combat. This review demonstrates the viability of targeting the GCX therapeutically, to support proper EC functionality and prevent and/or treat atherosclerosis.

Indexed as

AnimalsAtherosclerosisEndothelial CellsEndothelium, VascularGlycocalyxHumansModels, AnimalMolecular Targeted TherapyAtherosclerosisCardiovascular disease treatmentEndothelial dysfunctionEndothelial glycocalyx

Identifiers

PMID29127504
PMCPMC5681608
OpenAlexW2767573195

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.