Evidence map›Paper›PMID 34207084›Full record

ArticleInternational journal of molecular sciences2021

Methylglyoxal-Derived Advanced Glycation End Product (AGE4)-Induced Apoptosis Leads to Mitochondrial Dysfunction and Endoplasmic Reticulum Stress through the RAGE/JNK Pathway in Kidney Cells.

So-Ra Jeong, Kwang-Won Lee

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. 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
3.1field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Methylglyoxal Formation-Metabolic Routes and Consequences.Antioxidants (Basel, Switzerland) · 2025
    Review
  5. Article
  6. Article
  7. A Role for Advanced Glycation End Products in Molecular Ageing.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
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 at 1 institution in 1 country.

So-Ra JeongDepartment of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Anam-Dong, Sungbuk-Gu, Seoul 02841, Korea.
Kwang-Won LeeDepartment of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Anam-Dong, Sungbuk-Gu, Seoul 02841, Korea.ORCID 0000-0001-5326-469X
Korea University · KR

Funding

Korea Food Research Institute E0164400-04Korea University Research Grant K1516071
6 · The paper itself

Abstract

Advanced glycation end products (AGEs) are formed via nonenzymatic reactions between reducing sugars and proteins. Recent studies have shown that methylglyoxal, a potent precursor for AGEs, causes a variety of biological dysfunctions, including diabetes, inflammation, renal failure, and cancer. However, little is known about the function of methylglyoxal-derived AGEs (AGE4) in kidney cells. Therefore, we verified the expression of endoplasmic reticulum (ER) stress-related genes and apoptosis markers to determine the effects of AGE4 on human proximal epithelial cells (HK-2). Moreover, our results showed that AGE4 induced the expression of apoptosis markers, such as Bax, p53, and kidney injury molecule-1, but downregulated Bcl-2 and cyclin D1 levels. AGE4 also promoted the expression of NF-κB, serving as a transcription factor, and the phosphorylation of c-Jun NH

Indexed as

ApoptosisEndoplasmic Reticulum StressSignal TransductionAnimalsCell Cycle CheckpointsCell LineEpithelial CellsGlycation End Products, AdvancedHumansJNK Mitogen-Activated Protein KinasesKidneyMiceMitochondriaModels, BiologicalNF-kappa BPyruvaldehydeGlycation End Products, AdvancedJNK Mitogen-Activated Protein KinasesNF-kappa BPyruvaldehydeReactive Oxygen SpeciesTranscription Factorsendoplasmic reticulum stressJNK signal pathwaykidney injurymethylglyoxal-derived AGEsmitochondrial dysfunction

Identifiers

PMID34207084
PMCPMC8235496
OpenAlexW3177289139

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.