Evidence map›Paper›PMID 29499356›Full record

ReviewMatrix biology : journal of the International Society for Matrix Biology2018

A role for proteoglycans in vascular disease.

Thomas N Wight

Open access · greenAbstract readReview
In one paragraph

Review in Matrix biology : journal of the International Society for Matrix Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed, 1 pooled it
7.1field-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

92 citing papers in PubMed, 1 synthesis or guideline pooled it, 155 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Glycosaminoglycans as Polyelectrolytes: Charge, Interactions, and Applications.Chembiochem : a European journal of chemical biology · 2025
    Review
  12. Article
  13. Review
  14. Review
  15. Transport across the thoracic aortic wall: implications for aneurysm pathobiology, diagnosis, and treatment.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Biglycan stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article

32 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

1 author at 1 institution in 1 country.

Thomas N WightMatrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA 98101, United States. Electronic address: twight@benaroyaresearch.org.
Pearson (United States) · US

Funding

VLA-4 and VCAM-1 in Advanced AtherosclerosisP01HL018645 · NHLBI · UNIVERSITY OF WASHINGTON · PI RAINES, ELAINE W · 1985 to 2010
$23.9M
Role of Serum Amyloid A in Diabetic Vascular DiseaseP01HL092969 · NHLBI · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E. · 2008 to 2019
$23.5M
Defining the role of altered cytokine signaling pathways on autoimmunityU01AI101990 · NIAID · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BUCKNER, JANE HOYT · 2012 to 2016
$12.1M
Engineered Cardiac Morphogenesis-Stem Cells and ScaffoldsR01HL064387 · NHLBI · UNIVERSITY OF WASHINGTON · PI RATNER, BUDDY D · 2006 to 2010
$10.2M
Humna ES Cells for Cardiac Tissue EngineeringR24HL064387 · NHLBI · UNIVERSITY OF WASHINGTON · PI RATNER, BUDDY D · 2000 to 2004
$9.4M
Regulation of the Innate Immune Response by the Epithelium in AsthmaU19AI125378 · NIAID · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI HALLSTRAND, TEAL S · 2016 to 2020
$9.2M
NHLBI NIH HHS P01 HL018645NHLBI NIH HHS P01 HL092969NHLBI NIH HHS R01 HL064387NHLBI NIH HHS R24 HL064387NIAID NIH HHS U01 AI101990NIAID NIH HHS U19 AI125378
6 · The paper itself

Abstract

The content of proteoglycans (PGs) is low in the extracellular matrix (ECM) of vascular tissue, but increases dramatically in all phases of vascular disease. Early studies demonstrated that glycosaminoglycans (GAGs) including chondroitin sulfate (CS), dermatan sulfate (DS), keratan sulfate (KS) and heparan sulfate (HS) accumulate in vascular lesions in both humans and in animal models in areas of the vasculature that are susceptible to disease initiation (such as at branch points) and are frequently coincident with lipid deposits. Later studies showed the GAGs were covalently attached to specific types of core proteins that accumulate in vascular lesions. These molecules include versican (CSPG), biglycan and decorin (DS/CSPGs), lumican and fibromodulin (KSPGs) and perlecan (HSPG), although other types of PGs are present, but in lesser quantities. While the overall molecular design of these macromolecules is similar, there is tremendous structural diversity among the different PG families creating multiple forms that have selective roles in critical events that form the basis of vascular disease. PGs interact with a variety of different molecules involved in disease pathogenesis. For example, PGs bind and trap serum components that accumulate in vascular lesions such as lipoproteins, amyloid, calcium, and clotting factors. PGs interact with other ECM components and regulate, in part, ECM assembly and turnover. PGs interact with cells within the lesion and alter the phenotypes of both resident cells and cells that invade the lesion from the circulation. A number of therapeutic strategies have been developed to target specific PGs involved in key pathways that promote vascular disease. This review will provide a historical perspective of this field of research and then highlight some of the evidence that defines the involvement of PGs and their roles in the pathogenesis of vascular disease.

Indexed as

AnimalsExtracellular MatrixGlycosaminoglycansHumansMolecular Targeted TherapyProteoglycansSignal TransductionVascular DiseasesGlycosaminoglycansProteoglycansBiglycanDecorinFibromodulinLumicanPerlecanVascular diseaseVersican

Identifiers

PMID29499356
PMCPMC6110991
OpenAlexW2790164154

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.