Evidence map›Paper›PMID 27270766›Full record

ReviewGlycoconjugate journal2016

Diabetic kidney disease: a role for advanced glycation end-product receptor 1 (AGE-R1)?

Aowen Zhuang, Josephine M Forbes

Abstract readReview
PubMed Publisher
In one paragraph

Review in Glycoconjugate journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. A Role for Advanced Glycation End Products in Molecular Ageing.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. 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

2 authors.

Aowen ZhuangGlycation and Diabetes Group, Mater Research Institute, Translational Research Institute, The University of Queensland, South Brisbane, Queensland, Australia.
Josephine M ForbesGlycation and Diabetes Group, Mater Research Institute, Translational Research Institute, The University of Queensland, South Brisbane, Queensland, Australia. josephine.forbes@mater.uq.edu.au.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic patients are postulated to be in a perpetual state of oxidative stress and inflammation at sites where chronic complications occur. The accumulation of AGEs derived from both endogenous and exogenous sources (such as the diet) have been implicated in the development and progression of diabetic complications, particularly nephropathy. There has been some interest in investigating the potential for reducing the AGE burden in chronic disease, through the action of AGE "clearance" receptors, such as the advanced glycation end-product receptor 1 (AGE-R1). Reducing the burden of AGEs has been linked to attenuation of inflammation, slower progression of diabetic complications (in particular vascular and renal complications) and has been shown to extend lifespan. To date, however, there have been no direct investigations into whether AGE-R1 has any role in modulating normal kidney function, or specifically during the development and progression of diabetes. This mini-review will focus on the recent advances in knowledge around the mechanistic function of AGE-R1 and the implications of this for the pathogenesis of diabetic kidney disease.

Indexed as

AnimalsDiabetic NephropathiesGlycation End Products, AdvancedHumansReceptor for Advanced Glycation End ProductsAGER protein, humanGlycation End Products, AdvancedReceptor for Advanced Glycation End ProductsAGE-R1AGEsDiabetesDiabetic kidney diseaseDiabetic nephropathyOST-48

Identifiers

PMID27270766

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.