Evidence map›Paper›PMID 19662229›Full record

ArticleBiomarker insights2008

Changes in Hyaluronan Metabolism and RHAMM Receptor Expression Accompany Formation of Complicated Carotid Lesions and May be Pro-Angiogenic Mediators of Intimal Neovessel Growth.

Jerzy Krupinski, Priya Ethirajan, M Angels Font, Marta Miguel Turu, John Gaffney, Pat Kumar, Mark Slevin

Open access · greenAbstract read
In one paragraph

Article in Biomarker insights, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.1field-weighted citation impact, top 50% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Knockdown of CD44 expression decreases valve interstitial cell calcification in vitro.American journal of physiology. Heart and circulatory physiology · 2019
    Article
  3. The CD44-HA axis and inflammation in atherosclerosis: A temporal perspective.Matrix biology : journal of the International Society for Matrix Biology · 2019
    Review
  4. Article
  5. Dysregulation of hyaluronan homeostasis during aortic valve disease.Matrix biology : journal of the International Society for Matrix Biology · 2017
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
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

7 authors at 1 institution in 1 country.

Jerzy KrupinskiDepartment of Neurology, Stroke Unit, Hospital Universitari de Bellvitge (HUB), and IDIBELL, Barcelona, Spain.
Priya Ethirajan
M Angels Font
Marta Miguel Turu
John Gaffney
Pat Kumar
Mark Slevin
Bellvitge University Hospital · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have shown that changes in expression of the glycosaminoglycan, hyaluronan (HA) were associated with erosion in areas of post-mortem coronary artery liable to rupture. Angiogenesis is an important feature of ulcerating haemorrhagic plaques prone to rupture. HA is a glycosaminoglycan known to possess potent angiogenic properties on metabolism to oligosaccharides of HA (o-HA) in the presence of hyaluronidase (HYAL) enzymes. In this study, we have examined HA receptor and HYAL enzyme expression in a series of carotid artery specimens used as vascular transplants and exhibiting various stages of atherosclerotic lesions as determined by anatomo-pathology. Our results demonstrated dramatically increased expression of HYAL-1 in regions of inflammation associated with complicated plaques. Receptor for HA-mediated motility (RHAMM), which is known to be important in transducing angiogenic signals in vascular endothelium, was strongly expressed on intimal blood vessels from complicated lesions but almost absent from other regions including adventitial vessels. Metabolism of HA, together with up-regulation of RHAMM in complicated plaque lesions might be partly responsible for over-production of leaky neovessels and predisposition to plaque rupture.

Indexed as

angiogenesisatherosclerosisHyaluronanRHAMM

Identifiers

PMID19662229
PMCPMC2717833
OpenAlexW1736686524

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.