Evidence map›Paper›PMID 30279139›Full record

ReviewBiochimica et biophysica acta. Molecular basis of disease2018

Mechanistic targeting of advanced glycation end-products in age-related diseases.

Sheldon Rowan, Eloy Bejarano, Allen Taylor

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta. Molecular basis of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
11.3field-weighted citation impact, top 1% 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

96 citing papers in PubMed, 1 synthesis or guideline pooled it, 207 citations in OpenAlex.

  1. Host insulin resistance caused byFrontiers in cellular and infection microbiology · 2023
    Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Methylglyoxal Formation-Metabolic Routes and Consequences.Antioxidants (Basel, Switzerland) · 2025
    Review
  18. Article
  19. Review
  20. Review

36 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Sheldon RowanLaboratory for Nutrition and Vision Research, USDA Human Nutrition Research Center on Aging, Tufts University, 711 Washington St, Boston, MA 02111, USA.
Eloy BejaranoLaboratory for Nutrition and Vision Research, USDA Human Nutrition Research Center on Aging, Tufts University, 711 Washington St, Boston, MA 02111, USA.
Allen TaylorLaboratory for Nutrition and Vision Research, USDA Human Nutrition Research Center on Aging, Tufts University, 711 Washington St, Boston, MA 02111, USA. Electronic address: allen.taylor@tufts.edu.
Tufts University · US

Funding

Ubiquitin Function In Eye LensR01EY013250 · NEI · TUFTS UNIVERSITY BOSTON · PI TAYLOR, ALLEN · 2001 to 2012
$4.0M
Ubiquitin function in eye lensR01EY026979 · NEI · TUFTS UNIVERSITY BOSTON · PI TAYLOR, ALLEN · 2016 to 2018
$1.2M
Mechanistically linking AMD, glycemic index and protein homeostasisR01EY021212 · NEI · TUFTS UNIVERSITY BOSTON · PI TAYLOR, ALLEN · 2011 to 2013
$1.2M
NEI NIH HHS R01 EY013250NEI NIH HHS R01 EY021212NEI NIH HHS R01 EY026979
6 · The paper itself

Abstract

Glycative stress, caused by the accumulation of cytotoxic and irreversibly-formed sugar-derived advanced glycation end-products (AGEs), contributes to morbidity associated with aging, age-related diseases, and metabolic diseases. In this review, we summarize pathways leading to formation of AGEs, largely from sugars and glycolytic intermediates, and discuss detoxification of AGE precursors, including the glyoxalase system and DJ-1/Park7 deglycase. Disease pathogenesis downstream of AGE accumulation can be cell autonomous due to aggregation of glycated proteins and impaired protein function, which occurs in ocular cataracts. Extracellular AGEs also activate RAGE signaling, leading to oxidative stress, inflammation, and leukostasis in diabetic complications such as diabetic retinopathy. Pharmaceutical agents have been tested in animal models and clinically to diminish glycative burden. We summarize existing strategies and point out several new directions to diminish glycative stress including: plant-derived polyphenols as AGE inhibitors and glyoxalase inducers; improved dietary patterns, particularly Mediterranean and low glycemic diets; and enhancing proteolytic capacities of the ubiquitin-proteasome and autophagy pathways that are involved in cellular clearing of AGEs.

Indexed as

AnimalsAutophagyCataractDiabetic RetinopathyDrug DiscoveryGlycation End Products, AdvancedHumansMacular DegenerationReceptor for Advanced Glycation End ProductsUbiquitinGlycation End Products, AdvancedReceptor for Advanced Glycation End ProductsUbiquitinAdvanced glycation end-productsAge-related macular degenerationAutophagyCataractDiabetesDiabetic retinopathyGlyoxalaseRAGEUbiquitin-proteasome system

Identifiers

PMID30279139
PMCPMC6822271
OpenAlexW2889082981

What OpenQuestion holds

Textmetadata
LicenceTDM
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.