Evidence map›Paper›PMID 27766267›Full record

ArticleAorta (Stamford, Conn.)2016

Advanced Glycation End Products and its Soluble Receptors in the Pathogenesis of Thoracic Aortic Aneurysm.

Kailash Prasad, Abdullah Sarkar, Mohammad A Zafar, Ahmed Shoker, Hamdi Ei Moselhi, Maryann Tranquilli, Bulat A Ziganshin, John A Elefteriades

Open access · hybridAbstract read
In one paragraph

Article in Aorta (Stamford, Conn.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Involvement of AGE and Its Receptors in the Pathogenesis of Hypertension in Elderly People and Its Treatment.The International journal of angiology : official publication of the International College of Angiology, Inc · 2022
    Article
  6. Article
  7. Review
  8. Article
  9. AGE-RAGE Stress and Coronary Artery Disease.The International journal of angiology : official publication of the International College of Angiology, Inc · 2021
    Review
  10. Review
  11. Article
  12. Review
  13. The genetics and biomechanics of thoracic aortic diseases.Vascular biology (Bristol, England) · 2019
    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

8 authors at 4 institutions in 4 countries.

Kailash PrasadDepartment of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Abdullah SarkarAortic Institute at Yale-New Haven, Yale University School of Medicine, Connecticut, USA; College of Medicine, Alfaisal University, Ryadh, Saudi Arabia.
Mohammad A ZafarAortic Institute at Yale-New Haven, Yale University School of Medicine, Connecticut, USA.
Ahmed ShokerDepartment of Medicine, Royal University Hospital, Saskatoon, Saskatchewan, Canada.
Hamdi Ei MoselhiDepartment of Medicine, Royal University Hospital, Saskatoon, Saskatchewan, Canada.
Maryann TranquilliAortic Institute at Yale-New Haven, Yale University School of Medicine, Connecticut, USA.
Bulat A ZiganshinAortic Institute at Yale-New Haven, Yale University School of Medicine, Connecticut, USA; Department of Surgical Diseases #2, Kazan State Medical University, Kazan, Russia.
John A ElefteriadesAortic Institute at Yale-New Haven, Yale University School of Medicine, Connecticut, USA.
Yale University · USRoyal University Hospital · CAKazan State Medical University · RUUniversity of Saskatchewan · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMatrix metalloproteinases (MMPs) have been implicated in the pathogenesis of thoracic aortic aneurysms (TAAs). Cytokines [Interleukin (IL)-Iβ, IL-2, IL-6, and TNF-α)] increase the expression of MMP-2 and -3. Advanced glycation end products (AGEs) interact with cell receptors to increase the release of cytokines. Circulating soluble receptors for AGEs (sRAGE) and endogenous secretory RAGE (esRAGE) compete with membrane bound RAGE for binding with AGEs and reduce the production of cytokines. It is hypothesized that low levels of serum sRAGE and esRAGE and high levels of AGEs, AGEs/sRAGE, and AGEs/esRAGE would increase the levels of cytokines that would increase the levels MMPs, thus contributing to the formation of TAAs.

methodsThe study population was composed of 17 control subjects and 20 patients with TAA. Blood samples were collected for measurement of serum sRAGE, esRAGE, AGEs, cytokines, and MMPs. AGEs, sRAGE, and esRAGE were measured using ELISA kits, whereas the remaining parameters were measured using the Luminex Multi-Analyte system.

resultsThe levels of sRAGE were lower, while the levels of AGEs, AGEs/sRAGE, AGEs/esRAGE, cytokines and MMPs were higher in patients with TAA compared to controls. The levels of sRAGE were inversely correlated with cytokines and MMPs, while AGEs, AGEs/sRAGE and AGEs/esRAGE were positively correlated with cytokines and MMPs. Cytokines were positively correlated with MMPs.

conclusionsThe data suggest that the AGE-RAGE axis may be involved in the pathogenesis of TAA and that low levels of sRAGE and high levels of AGEs, AGEs/sRAGE, and AGEs/esRAGE are risk factors for TAA.

Indexed as

Advanced glycation end productsAortic aneurysmCytokinesMatrix metalloproteinaseSoluble RAGEThoracic aortic aneurysm

Identifiers

PMID27766267
PMCPMC5068493
OpenAlexW2342684693

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.