Evidence map›Paper›PMID 37227674›Full record

ArticleMolecular biology reports2023

Glycolaldehyde-derived advanced glycation end products promote macrophage proliferation via the JAK-STAT signaling pathway.

Takao Toyomura, Masahiro Watanabe, Hidenori Wake, Takashi Nishinaka, Omer Faruk Hatipoglu, Hideo Takahashi, Masahiro Nishibori, Shuji Mori

Abstract read
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In one paragraph

Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Progression in the In Vitro Macrophage Expansion.Journal of immunology research · 2025
    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 3 institutions in 1 country.

Takao ToyomuraDepartment of Pharmacology, School of Pharmacy, Shujitsu University, Nishigawara, Naka-ku, Okayama, 703-8516, Japan.
Masahiro WatanabeDepartment of Pharmacology, School of Pharmacy, Shujitsu University, Nishigawara, Naka-ku, Okayama, 703-8516, Japan.
Hidenori WakeDepartment of Pharmacology, Faculty of Medicine, Kindai University, Osaka-Sayama, 589-8511, Japan.
Takashi NishinakaDepartment of Pharmacology, Faculty of Medicine, Kindai University, Osaka-Sayama, 589-8511, Japan.
Omer Faruk HatipogluDepartment of Pharmacology, Faculty of Medicine, Kindai University, Osaka-Sayama, 589-8511, Japan.
Hideo TakahashiDepartment of Pharmacology, Faculty of Medicine, Kindai University, Osaka-Sayama, 589-8511, Japan.
Masahiro NishiboriDepartment of Pharmacology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine, Okayama, 700-8558, Japan.
Shuji MoriDepartment of Pharmacology, School of Pharmacy, Shujitsu University, Nishigawara, Naka-ku, Okayama, 703-8516, Japan. morimori@shujitsu.ac.jp.ORCID http://orcid.org/0000-0002-2826-1937
Kindai University · JPShujitsu University · JPOkayama University · JP

Funding

JSPS KAKENHI 21K06657JSPS KAKENHI 21K06701
6 · The paper itself

Abstract

backgroundAdvanced glycation end products (AGEs) are heterogeneous proinflammatory molecules produced by a non-enzymatic glycation reaction between reducing sugars (and their metabolites) and biomolecules with amino groups, such as proteins. Although increases in and the accumulation of AGEs have been implicated in the onset and exacerbation of lifestyle- or age-related diseases, including diabetes, their physiological functions have not yet been elucidated in detail. METHODS AND

resultsThe present study investigated the cellular responses of the macrophage cell line RAW264.7 stimulated by glycolaldehyde-derived AGEs (Glycol-AGEs) known as representative toxic AGEs. The results obtained showed that Glycol-AGEs significantly promoted the proliferation of RAW264.7 cells at a low concentration range (1-10 µg/mL) in a concentration-dependent manner. On the other hand, neither TNF-α production nor cytotoxicity were induced by the same concentrations of Glycol-AGEs. The increases observed in cell proliferation by low concentrations of Glycol-AGEs were also detected in receptor triple knockout (RAGE-TLR4-TLR2 KO) cells as well as in wild-type cells. Increases in cell proliferation were not affected by various kinase inhibitors, including MAP kinase inhibitors, but were significantly suppressed by JAK2 and STAT5 inhibitors. In addition, the expression of some cell cycle-related genes was up-regulated by the stimulation with Glycol-AGEs.

conclusionsThese results suggest a novel physiological role for AGEs in the promotion of cell proliferation via the JAK-STAT pathway.

Indexed as

Glycation End Products, AdvancedSignal TransductionAcetaldehydeCell ProliferationJanus KinasesMacrophagesReceptor for Advanced Glycation End ProductsSTAT Transcription FactorsAcetaldehydeGlycation End Products, AdvancedglycolaldehydeJanus KinasesReceptor for Advanced Glycation End ProductsSTAT Transcription FactorsAdvanced glycation end productsDamage-associated molecular pattern moleculesPromoted cell proliferation

Identifiers

PMID37227674
OpenAlexW4378172194

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.