Evidence map›Paper›PMID 30794349›Full record

ArticleAging cell2019

Knockout of receptor for advanced glycation end-products attenuates age-related renal lesions.

Thibault Teissier, Valentine Quersin, Viviane Gnemmi, Maité Daroux, Mike Howsam, Florian Delguste, Cécile Lemoine, Chantal Fradin, Ann-Marie Schmidt, Christelle Cauffiez and 5 more

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  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

15 authors at 6 institutions in 2 countries.

Thibault TeissierU995 - Lille Inflammation Research International Center, INSERM, CHU Lille, University of Lille, Lille, France.
Valentine QuersinU995 - Lille Inflammation Research International Center, INSERM, CHU Lille, University of Lille, Lille, France.
Viviane GnemmiDepartment of Pathology, U1172 - Jean-Pierre Aubert Research Center, INSERM, CHU Lille, University of Lille, Lille, France.
Maité DarouxU995 - Lille Inflammation Research International Center, INSERM, CHU Lille, University of Lille, Lille, France.
Mike HowsamU995 - Lille Inflammation Research International Center, INSERM, CHU Lille, University of Lille, Lille, France.
Florian DelgusteU995 - Lille Inflammation Research International Center, INSERM, CHU Lille, University of Lille, Lille, France.
Cécile LemoineU995 - Lille Inflammation Research International Center, INSERM, CHU Lille, University of Lille, Lille, France.
Chantal FradinU995 - Lille Inflammation Research International Center, INSERM, CHU Lille, University of Lille, Lille, France.
Ann-Marie SchmidtDepartment of Medicine, Diabetes Research Center, NYU Langone Medical Center, New York, New York.
Christelle CauffiezEA4483 IMPECS-IMPact of Environmental ChemicalS on Human Health, CHU Lille, University of Lille, Lille, France.
Thierry BrousseauUF8832 - Biochimie Automatisée, Pôle de Biologie Pathologie Génétique, CHU Lille, Lille, France.
François GlowackiDepartment of Nephrology, CHU Lille, Lille, France.
Frédéric J TessierU995 - Lille Inflammation Research International Center, INSERM, CHU Lille, University of Lille, Lille, France.
Eric BoulangerU995 - Lille Inflammation Research International Center, INSERM, CHU Lille, University of Lille, Lille, France.
Marie FrimatU995 - Lille Inflammation Research International Center, INSERM, CHU Lille, University of Lille, Lille, France.
Centre Hospitalier Universitaire de Lille · FRInserm · FRLille Inflammation Research International Center · FRUniversité de Lille · FRInstitut de Biologie de Lille · FRNYU Langone Health · US

Funding

Digest Science foundationInstitut National de la Santé et de la Recherche Médicale
6 · The paper itself

Abstract

Pro-aging effects of endogenous advanced glycation end-products (AGEs) have been reported, and there is increasing interest in the pro-inflammatory and -fibrotic effects of their binding to RAGE (the main AGE receptor). The role of dietary AGEs in aging remains ill-defined, but the predominantly renal accumulation of dietary carboxymethyllysine (CML) suggests the kidneys may be particularly affected. We studied the impact of RAGE invalidation and a CML-enriched diet on renal aging. Two-month-old male, wild-type (WT) and RAGE

Indexed as

AgingAnimalsKidney DiseasesMaleMiceMice, Inbred C57BLMice, KnockoutReceptor for Advanced Glycation End ProductsAger protein, mouseReceptor for Advanced Glycation End Productsadvanced glycation end-productsamyloidosischronic kidney diseasenephrosclerosisreceptor for AGEsrenal aging

Identifiers

PMID30794349
PMCPMC6413655
OpenAlexW2916357426

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.