Evidence map›Paper›PMID 30014569›Full record

ArticleCell proliferation2018

Blockade of receptors of advanced glycation end products ameliorates diabetic osteogenesis of adipose-derived stem cells through DNA methylation and Wnt signalling pathway.

Maorui Zhang, Yong Li, Pengcheng Rao, Kui Huang, Daowen Luo, Xiaoxiao Cai, Jingang Xiao

Abstract read
In one paragraph

Article in Cell proliferation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
–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

39 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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  4. Article
  5. Review
  6. Wnt/β-Catenin Signaling in Diabetic Complications: Mechanisms and Therapeutic Potential.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Review
  7. Observational
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  9. Review
  10. Review
  11. Article
  12. Article
  13. Effects of advanced glycation end products on stem cell.Frontiers in cell and developmental biology · 2024
    Review
  14. Review
  15. Review
  16. Article
  17. Article
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  19. Article
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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

7 authors.

Maorui ZhangDepartment of Oral Implantology, The Affiliated Stomatology Hospital of Southwest Medical University, Luzhou, China.
Yong LiDepartment of Oral Implantology, The Affiliated Stomatology Hospital of Southwest Medical University, Luzhou, China.
Pengcheng RaoOrofacial Reconstruction and Regeneration Laboratory, The Affiliated Stomatology Hospital of Southwest Medical University, Luzhou, China.
Kui HuangOrofacial Reconstruction and Regeneration Laboratory, The Affiliated Stomatology Hospital of Southwest Medical University, Luzhou, China.
Daowen LuoOrofacial Reconstruction and Regeneration Laboratory, The Affiliated Stomatology Hospital of Southwest Medical University, Luzhou, China.
Xiaoxiao CaiState Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Jingang XiaoDepartment of Oral Implantology, The Affiliated Stomatology Hospital of Southwest Medical University, Luzhou, China.ORCID http://orcid.org/0000-0003-1300-7191

Funding

Joint project of Luzhou Municipal People's Government and Southwest Medical University 2015LZCYD-S05(2/12)National Natural Science Foundation of China 81371125National Natural Science Foundation of China 81471803Program of Science & Technology Department of Sichuan Province 2014JY0044
6 · The paper itself

Abstract

objectivesDiabetes mellitus-related osteoporosis is caused by the imbalance between bone absorption and bone formation. Advanced glycation end products (AGEs) are considered a cause of diabetic osteoporosis. Although adipose-derived stem cells (ASCs) are promising adult stem cells in bone tissue regeneration, the ability of osteogenesis of ASCs in diabetic environment needs to explore. This study aimed to investigate the influence of AGEs on the osteogenic potential of ASCs and to explore the signalling pathways involved in its effect. MATERIALS AND

methodsASCs were isolated from inguinal fat and cultured in osteogenic media with or without AGEs and FPS-ZM1, an inhibitor of receptor for AGEs (RAGE). Alizarin red-S, Oil Red-O and Alcian blue staining were used to confirm osteogenic, adipogenic and chondrogenic potential of ASCs, respectively. Immunofluorescence, western blotting and real-time PCR were used to measure changes in markers of osteogenic differentiation, DNA methylation and Wnt signalling.

resultsThe multipotentiality of ASCs was confirmed. Treated with AGEs, OPN and RUNX2 expressions of ASCs were reduced and there was a noticeable loss of mineralization, concomitant with an increase in the expression of RAGE, 5-MC, DNMT1 and DNMT3a. AGEs treatment also led to a loss of Wnt signalling pathway markers, including β-Catenin and LEF1, with an increase in GSK-3β. Treatment with the RAGE inhibitor, FPS-ZM1, rescued AGEs-induced loss of osteogenic potential, modulated DNA methylation and upregulated Wnt signalling in ASCs.

conclusionsOur results demonstrate that AGEs-RAGE signalling inhibits the osteogenic potential of ASCs under osteoinductive conditions by modulating DNA methylation and Wnt signalling. FPS-ZM1 can rescue the negative effects of AGEs and provide a possible treatment for bone tissue regeneration in patients with diabetic osteoporosis.

Indexed as

AdipocytesAdipogenesisAdipose TissueAdult Stem CellsAnimalsBone and BonesBone RegenerationCell DifferentiationCells, CulturedDiabetes MellitusDNA MethylationFemaleGlycation End Products, AdvancedGlycogen Synthase Kinase 3 betaOsteogenesisOsteoporosisGlycation End Products, AdvancedGlycogen Synthase Kinase 3 betaReceptor for Advanced Glycation End Products

Identifiers

PMID30014569
PMCPMC6528890

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.