Evidence map›Paper›PMID 36359899›Full record

ReviewCells2022

Advanced Glycation End Products and Inflammation in Type 1 Diabetes Development.

Chenping Du, Rani O Whiddett, Irina Buckle, Chen Chen, Josephine M Forbes, Amelia K Fotheringham

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

25 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Interaction between diabetes and osteoporosis: imbalance between inflammation and bone remodeling.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2025
    Review
  5. Article
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  7. [Elevated advanced glycation endproducts is a risk factor for stenosis after primary arteriovenous fistula surgery].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  8. Review
  9. Narra J · 2025
    Article
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  13. Observational
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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

6 authors at 2 institutions in 1 country.

Chenping DuGlycation and Diabetes Complications Group, Mater Research Institute-The University of Queensland, Translational Research Institute, Woolloongabba 4102, Australia.
Rani O WhiddettGlycation and Diabetes Complications Group, Mater Research Institute-The University of Queensland, Translational Research Institute, Woolloongabba 4102, Australia.ORCID 0000-0002-5459-5519
Irina BuckleGlycation and Diabetes Complications Group, Mater Research Institute-The University of Queensland, Translational Research Institute, Woolloongabba 4102, Australia.ORCID 0000-0002-7486-3509
Chen ChenSchool of Biomedical Sciences, Faculty of Medicine, The University of Queensland, St Lucia 4072, Australia.ORCID 0000-0003-2104-534X
Josephine M ForbesGlycation and Diabetes Complications Group, Mater Research Institute-The University of Queensland, Translational Research Institute, Woolloongabba 4102, Australia.ORCID 0000-0002-5595-8174
Amelia K FotheringhamGlycation and Diabetes Complications Group, Mater Research Institute-The University of Queensland, Translational Research Institute, Woolloongabba 4102, Australia.ORCID 0000-0002-3213-8923
Translational Research Institute · AUThe University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes (T1D) is an autoimmune disease in which the β-cells of the pancreas are attacked by the host's immune system, ultimately resulting in hyperglycemia. It is a complex multifactorial disease postulated to result from a combination of genetic and environmental factors. In parallel with increasing prevalence of T1D in genetically stable populations, highlighting an environmental component, consumption of advanced glycation end products (AGEs) commonly found in in Western diets has increased significantly over the past decades. AGEs can bind to cell surface receptors including the receptor for advanced glycation end products (RAGE). RAGE has proinflammatory roles including in host-pathogen defense, thereby influencing immune cell behavior and can activate and cause proliferation of immune cells such as islet infiltrating CD8

Indexed as

Diabetes Mellitus, Type 1HyperglycemiaGlycation End Products, AdvancedHumansInflammationReceptor for Advanced Glycation End ProductsGlycation End Products, AdvancedReceptor for Advanced Glycation End Productsautoimmunitydietary AGEsRAGEtype 1 diabetes

Identifiers

PMID36359899
PMCPMC9657002
OpenAlexW4308475615

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.