Evidence map›Paper›PMID 25595716›Full record

ArticleRNA (New York, N.Y.)2015

MicroRNA-130a can inhibit hepatitis B virus replication via targeting PGC1α and PPARγ.

Jyun-Yuan Huang, Shu-Fan Chou, Jun-Wei Lee, Hung-Lin Chen, Chun-Ming Chen, Mi-Hua Tao, Chiaho Shih

Abstract read
In one paragraph

Article in RNA (New York, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing 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

38 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Regulatory role of microRNAs in virus-mediated inflammation.Journal of inflammation (London, England) · 2024
    Review
  5. Identification ofAnimal biotechnology · 2024
    Article
  6. Article
  7. Review
  8. Article
  9. Cell death pathways and viruses: Role of microRNAs.Molecular therapy. Nucleic acids · 2021
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  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

7 authors.

Jyun-Yuan HuangGraduate Institute of Life Sciences, National Defense Medical Center, Taipei, 114 Taiwan Institute of Biomedical Sciences, Academia Sinica, Taipei, 115 Taiwan.
Shu-Fan ChouInstitute of Biomedical Sciences, Academia Sinica, Taipei, 115 Taiwan Graduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei, 110 Taiwan.
Jun-Wei LeeInstitute of Biomedical Sciences, Academia Sinica, Taipei, 115 Taiwan.
Hung-Lin ChenInstitute of Biomedical Sciences, Academia Sinica, Taipei, 115 Taiwan.
Chun-Ming ChenInstitute of Biomedical Sciences, Academia Sinica, Taipei, 115 Taiwan.
Mi-Hua TaoInstitute of Biomedical Sciences, Academia Sinica, Taipei, 115 Taiwan.
Chiaho ShihGraduate Institute of Life Sciences, National Defense Medical Center, Taipei, 114 Taiwan Institute of Biomedical Sciences, Academia Sinica, Taipei, 115 Taiwan cshih@ibms.sinica.edu.tw.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In hepatitis B virus (HBV)-replicating hepatocytes, miR-130a expression was significantly reduced. In a reciprocal manner, miR-130a reduced HBV replication by targeting at two major metabolic regulators PGC1α and PPARγ, both of which can potently stimulate HBV replication. We proposed a positive feed-forward loop between HBV, miR-130a, PPARγ, and PGC1α. Accordingly, HBV can significantly enhance viral replication by reducing miR-130a and increasing PGC1α and PPARγ. NF-κB/p65 can strongly stimulate miR-130a promoter, while miR-130a can promote NF-κB/p65 protein level by reducing PPARγ and thus NF-κB/p65 protein degradation. We postulated another positive feed-forward loop between miR-130a and NF-κB/p65 via PPARγ. During liver inflammation, NF-κB signaling could contribute to viral clearance via its positive effect on miR-130a transcription. Conversely, in asymptomatic HBV carriers, persistent viral infection could reduce miR-130a and NF-κB expression, leading to dampened inflammation and immune tolerance. Finally, miR-130a could contribute to metabolic homeostasis by dual targeting PGC1α and PPARγ simultaneously.

Indexed as

DNA ReplicationGene Expression RegulationHepatitis BHepatitis B virusHepatocytesHumansMicroRNAsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPAR gammaSignal TransductionTranscription FactorsVirus ReplicationMicroRNAsMIRN130 microRNA, humanPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPAR gammaPPARGC1A protein, humanTranscription Factorshepatitis B virusinflammationmicroRNAPGC1αPPARγ

Identifiers

PMID25595716
PMCPMC4338335

What OpenQuestion holds

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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.