Evidence map›Paper›PMID 26824050›Full record

ArticleJournal of diabetes research2016

Clopidogrel Protects Endothelium by Hindering TNFα-Induced VCAM-1 Expression through CaMKKβ/AMPK/Nrf2 Pathway.

Huabing Yang, Pengjun Zhao, Shiliu Tian

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Whole Exome Sequencing Study in a Family with Type 2 Diabetes Mellitus.International journal of general medicine · 2021
    Article
  9. Experimental and therapeutic medicine · 2020
    Article
  10. Article
  11. A Novel STAT3-Mediated GATA6 Pathway Contributes toOxidative medicine and cellular longevity · 2020
    Article
  12. Article
  13. Evidence for the important role of inflammation in xenotransplantation.Journal of inflammation (London, England) · 2019
    Review
  14. Luteolin activates ERK1/2- and CaInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    Article
  15. Article
  16. Article
  17. The Role of Nrf2 in Cardiovascular Function and Disease.Oxidative medicine and cellular longevity · 2017
    Review
  18. Impact ofFrontiers in pharmacology · 2016
    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

3 authors at 3 institutions in 2 countries.

Huabing YangSchool of Medical Sciences, Hubei University of Chinese Medicine, Wuhan 430065, China; Department of Medicine and Harold Hamm Oklahoma Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
Pengjun ZhaoPediatric Heart Center, Children's Hospital of Fudan University, Shanghai 200032, China.
Shiliu TianKey Laboratory of Exercise and Health Sciences of Ministry of Education, Shanghai University of Sport, Shanghai 200438, China.
Children's Hospital of Fudan University · CNHubei University of Chinese Medicine · CNShanghai University of Sport · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clopidogrel (INN), an oral antiplatelet drug, has been revealed to have a number of biological properties, for instance, anti-inflammation and antioxidation. Oxidative stress plays an imperative role in inflammation, diabetes mellitus, atherosclerosis, and cancer. In the present study, human aortic endothelial cells (HAECs) were employed to explore the anti-inflammatory activity of INN. INN reduced TNFα-induced reactive oxygen species (ROS) generation and time-dependently prompted the expression and activity of heme oxygenase 1 (HO-1). Cellular glutathione (GSH) levels were augmented by INN. shHO-1 blocked the INN suppression of TNFα-induced HL-60 cell adhesion. The CaMKKβ/AMPK pathway and Nrf2 transcriptional factor were implicated in the induction of HO-1 by INN. Additionally, TNFα dramatically augmented VCAM-1 expression at protein and mRNA levels. INN treatment strikingly repressed TNFα-induced expression of VCAM-1 and HL-60 cell adhesion. Compound C, an AMPK inhibitor, and shNrf2 abolished TNFα-induced expression of VCAM-1 and HL-60 cell adhesion. Our data suggest that INN diminishes TNFα-stimulated VCAM-1 expression at least in part via HO-1 induction, which is CaMKKβ/AMPK pathway-dependent.

Indexed as

AMP-Activated Protein KinasesAnti-Inflammatory AgentsAntioxidantsCalcium-Calmodulin-Dependent Protein Kinase KinaseCell AdhesionClopidogrelEndothelial CellsGlutathioneHeme Oxygenase-1HL-60 CellsHumansLeukocytesNF-E2-Related Factor 2Oxidative StressReactive Oxygen SpeciesRNA InterferenceAMP-Activated Protein KinasesAnti-Inflammatory AgentsAntioxidantsCalcium-Calmodulin-Dependent Protein Kinase KinaseCAMKK2 protein, humanClopidogrelGlutathioneHeme Oxygenase-1HMOX1 protein, humanNFE2L2 protein, humanNF-E2-Related Factor 2Reactive Oxygen SpeciesTiclopidineTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID26824050
PMCPMC4707324
OpenAlexW2245387273

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.