Evidence map›Paper›PMID 24407238›Full record

ArticleCell death & disease2014

Adenosine 5'-monophosphate ameliorates D-galactosamine/lipopolysaccharide-induced liver injury through an adenosine receptor-independent mechanism in mice.

Y Zhan, Z Wang, P Yang, T Wang, L Xia, M Zhou, Y Wang, S Wang, Z Hua, J Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Selenium enrichment enhances the alleviating effect ofCurrent research in food science · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

10 authors at 3 institutions in 1 country.

Y ZhanCenter for Molecular Metabolism, Nanjing University of Science and Technology, Nanjing 210094, China.
Z WangEast Hospital, Tongji University, Shanghai 200120, China.
P YangCenter for Molecular Metabolism, Nanjing University of Science and Technology, Nanjing 210094, China.
T WangCenter for Molecular Metabolism, Nanjing University of Science and Technology, Nanjing 210094, China.
L XiaCenter for Molecular Metabolism, Nanjing University of Science and Technology, Nanjing 210094, China.
M ZhouCenter for Molecular Metabolism, Nanjing University of Science and Technology, Nanjing 210094, China.
Y WangCenter for Molecular Metabolism, Nanjing University of Science and Technology, Nanjing 210094, China.
S WangCenter for Molecular Metabolism, Nanjing University of Science and Technology, Nanjing 210094, China.
Z HuaThe State Kay Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, China.
J Zhang1] Center for Molecular Metabolism, Nanjing University of Science and Technology, Nanjing 210094, China [2] The State Kay Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, China.
Nanjing University of Science and Technology · CNNanjing University · CNShanghai East Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

D-galactosamine (GalN)/lipopolysaccharide (LPS)-induced lethality and acute liver failure is dependent on endogenously produced inflammatory cytokines. Adenosine has been proven to be a central role in the regulation of inflammatory response. It is not entirely clear that which adenosine action is actually crucial to limiting inflammatory tissue destruction. Here we showed that GalN/LPS challenge elevated hepatic adenosine and induced lethality in adenosine receptor-deficient mice with equal efficiency as wild-type mice. In GalN/LPS-treated mice, pretreatment with adenosine 5'-monophosphate (5'-AMP) significantly elevated hepatic adenosine level and reduced mortality through decreasing cytokine and chemokine production. In RAW264.7 cells, 5'-AMP treatment inhibited the production of inflammatory cytokines, which is not mediated through adenosine receptors. 5'-AMP failed to attenuate LPS-induced nuclear factor-κB (NF-κB) p65 nuclear translocation, but reduced LPS-induced recruitment of NF-κB p65 to inflammatory gene promoters and decreased LPS-induced enrichment of H3K4 dimethylation at the tumor necrosis factor-α (TNF-α) promoter, which was involved in 5'-AMP-induced elevation of cellular adenosine and a decline of methylation potential. In vitro biochemical analysis revealed that adenosine directly attenuated recruitment of NF-κB to the TNF-α and interleukin-6 promoters. Our findings demonstrate that 5'-AMP-inhibiting inflammatory response is not mediated by adenosine receptors and it may represent a potential protective agent for amelioration of LPS-induced liver injury.

Indexed as

Adenosine MonophosphateAnimalsChemical and Drug Induced Liver InjuryGalactosamineHumansLipopolysaccharidesLiverMaleMiceMice, Inbred C57BLNF-kappa BReceptors, Purinergic P1Tumor Necrosis Factor-alphaAdenosine MonophosphateGalactosamineLipopolysaccharidesNF-kappa BReceptors, Purinergic P1Tumor Necrosis Factor-alpha

Identifiers

PMID24407238
PMCPMC4040656
OpenAlexW1996871653

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.