Evidence map›Paper›PMID 39273671›Full record

ArticleInternational journal of molecular sciences2024

Glucose-Dependent Insulinotropic Polypeptide Inhibits AGE-Induced NADPH Oxidase-Derived Oxidative Stress Generation and Foam Cell Formation in Macrophages Partly via AMPK Activation.

Michishige Terasaki, Hironori Yashima, Yusaku Mori, Tomomi Saito, Naoto Inoue, Takanori Matsui, Naoya Osaka, Tomoki Fujikawa, Makoto Ohara, Sho-Ichi Yamagishi

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–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

14 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. The role of the incretin GIP in inflammation.Journal of endocrinological investigation · 2026
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. 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

10 authors.

Michishige TerasakiDivision of Diabetes, Metabolism, and Endocrinology, Department of Medicine, Graduate School of Medicine, Showa University, 1-5-8 Shinagawa, Tokyo 142-8666, Japan.ORCID 0000-0002-7405-7419
Hironori YashimaDivision of Diabetes, Metabolism, and Endocrinology, Department of Medicine, Graduate School of Medicine, Showa University, 1-5-8 Shinagawa, Tokyo 142-8666, Japan.
Yusaku MoriAnti-Glycation Research Section, Division of Diabetes, Metabolism, and Endocrinology, Department of Medicine, Graduate School of Medicine, Showa University, 1-5-8 Shinagawa, Tokyo 142-8666, Japan.ORCID 0000-0002-1734-0605
Tomomi SaitoDivision of Diabetes, Metabolism, and Endocrinology, Department of Medicine, Graduate School of Medicine, Showa University, 1-5-8 Shinagawa, Tokyo 142-8666, Japan.
Naoto InoueDivision of Diabetes, Metabolism, and Endocrinology, Department of Medicine, Graduate School of Medicine, Showa University, 1-5-8 Shinagawa, Tokyo 142-8666, Japan.
Takanori MatsuiDepartment of Bioscience and Biotechnology, Fukui Prefectural University, Eiheiji, Fukui 910-1195, Japan.ORCID 0000-0001-9506-7571
Naoya OsakaDivision of Diabetes, Metabolism, and Endocrinology, Department of Medicine, Graduate School of Medicine, Showa University, 1-5-8 Shinagawa, Tokyo 142-8666, Japan.
Tomoki FujikawaDivision of Diabetes, Metabolism, and Endocrinology, Department of Medicine, Graduate School of Medicine, Showa University, 1-5-8 Shinagawa, Tokyo 142-8666, Japan.
Makoto OharaDivision of Diabetes, Metabolism, and Endocrinology, Department of Medicine, Graduate School of Medicine, Showa University, 1-5-8 Shinagawa, Tokyo 142-8666, Japan.
Sho-Ichi YamagishiDivision of Diabetes, Metabolism, and Endocrinology, Department of Medicine, Graduate School of Medicine, Showa University, 1-5-8 Shinagawa, Tokyo 142-8666, Japan.ORCID 0000-0003-0102-0823

Funding

Japan Association for Diabetes Education and Care 2021-YNG-002Japan Society for the Promotion of Science 20K07075Japan Society for the Promotion of Science 24K09316Research Grant Award 2022 from the Japanese Society of Anti-Aging Medicine 2022-2
6 · The paper itself

Abstract

Glucose-dependent insulinotropic polypeptide (GIP) of the incretin group has been shown to exert pleiotropic actions. There is growing evidence that advanced glycation end products (AGEs), senescent macromolecules formed at an accelerated rate under chronic hyperglycemic conditions, play a role in the pathogenesis of atherosclerotic cardiovascular disease in diabetes. However, whether and how GIP could inhibit the AGE-induced foam cell formation of macrophages, an initial step of atherosclerosis remains to be elucidated. In this study, we address these issues. We found that AGEs increased oxidized low-density-lipoprotein uptake into reactive oxygen species (ROS) generation and

Indexed as

AMP-Activated Protein KinasesCyclin-Dependent Kinase 5Foam CellsGastric Inhibitory PolypeptideGlycation End Products, AdvancedNADPH OxidasesOxidative StressReactive Oxygen SpeciesCD36 AntigensHumansLipoproteins, LDLMacrophagesU937 CellsAMP-Activated Protein KinasesCD36 AntigensCDK5 protein, humanCyclin-Dependent Kinase 5Gastric Inhibitory PolypeptideGlycation End Products, AdvancedLipoproteins, LDLNADPH Oxidasesoxidized low density lipoproteinReactive Oxygen SpeciesAGEsAMPKCD36Cdk5GIPNADPH oxidase

Identifiers

PMID39273671
PMCPMC11395916

What Socratic 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 Socratic graph.