Evidence map›Paper›PMID 25059721›Full record

ArticleJournal of physiology and biochemistry2014

Tumor necrosis factor-α-induced nuclear factor-kappaB activation in human cardiomyocytes is mediated by NADPH oxidase.

Kyaw Thu Moe, Katwadi Khairunnisa, Nwe Oo Yin, Jaye Chin-Dusting, Philip Wong, Meng Cheong Wong

Abstract read
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In one paragraph

Article in Journal of physiology and biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 55 citations in OpenAlex.

  1. PD-1/PD-L1 Signaling in Non-ICI Myocarditis.JACC. Basic to translational science · 2026
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  5. Raspberry polyphenols target molecular pathways of heart failure.The Journal of nutritional biochemistry · 2024
    Article
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  10. Article
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  12. Review
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  15. Review
  16. Review
  17. A Comprehensive Review of the Potential Use of Green Tea Polyphenols in the Management of COVID-19.Evidence-based complementary and alternative medicine : eCAM · 2021
    Review
  18. Article
  19. Article
  20. 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

6 authors at 3 institutions in 2 countries.

Kyaw Thu MoeResearch and Development Unit, National Heart Centre Singapore, 7 Hospital Drive SingHealth Research Facilities Block A, #03-05, Singapore, 169611, Singapore, moe.kyaw.thu@nhcs.com.sg.
Katwadi Khairunnisa
Nwe Oo Yin
Jaye Chin-Dusting
Philip Wong
Meng Cheong Wong
National Heart Centre Singapore · SGBaker Heart and Diabetes Institute · AUNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An elevated level of tumor necrosis factor (TNF)-α is implicated in several cardiovascular diseases including heart failure. Numerous reports have demonstrated that TNF-α activates nuclear factor (NF)-kappaB, resulting in the upregulation of several genes that regulate inflammation, proliferation, and apoptosis of cardiomyocytes. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, a major source of reactive oxygen species (ROS), is also activated by TNF-α and plays a crucial role in redox-sensitive signaling pathways. The present study investigated whether NADPH oxidase mediates TNF-α-induced NF-kappaB activation and NF-kappaB-mediated gene expression. Human cardiomyocytes were treated with recombinant TNF-α with or without pretreatment with diphenyleneiodonium (DPI) and apocynin, inhibitors of NADPH oxidase. TNF-α-induced ROS production was measured using 5-(and-6)-chloromethyl-2', 7'-dichlorodihydrofluorescein diacetate assay. TNF-α-induced NF-kappaB activation was also examined using immunoblot; NF-kappaB binding to its binding motif was determined using a Cignal reporter luciferase assay and an electrophoretic mobility shift assay. TNF-α-induced upregulation of interleukin (IL)-1β and vascular cell adhesion molecule (VCAM)-1 was investigated using real-time PCR and immunoblot. TNF-α-induced ROS production in cardiomyocytes was mediated by NADPH oxidase. Phosphorylation of IKK-α/β and p65, degradation of IkappaBα, binding of NF-kappaB to its binding motif, and upregulation of IL-1β and VCAM-1 induced by TNF-α were significantly attenuated by treatment with DPI and apocynin. Collectively, these findings demonstrate that NADPH oxidase plays a role in regulation of TNF-α-induced NF-kappaB activation and upregulation of proinflammatory cytokines, IL-1β and VCAM-1, in human cardiomyocytes.

Indexed as

AcetophenonesCells, CulturedEnzyme InhibitorsHumansI-kappa B KinaseInterleukin-1betaMyocytes, CardiacNADPH OxidasesNF-kappa BOnium CompoundsPhosphorylationReactive Oxygen SpeciesRecombinant ProteinsSignal TransductionTumor Necrosis Factor-alphaUp-RegulationAcetophenonesacetovanillonediphenyleneiodoniumEnzyme InhibitorsI-kappa B KinaseInterleukin-1betaNADPH OxidasesNF-kappa BOnium CompoundsReactive Oxygen SpeciesRecombinant ProteinsTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID25059721
OpenAlexW2017045862

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.