Evidence map›Paper›PMID 25896250›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2015

Inhibition of Dexamethasone-induced Fatty Liver Development by Reducing miR-17-5p Levels.

William W Du, Fengqiong Liu, Sze Wan Shan, Xindi Cindy Ma, Shaan Gupta, Tianru Jin, David Spaner, Sergey N Krylov, Yaou Zhang, Wenhua Ling and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  3. Current strategies for nonalcoholic fatty liver disease treatment (Review).International journal of molecular medicine · 2024
    Review
  4. The effect ofResearch in pharmaceutical sciences · 2024
    Article
  5. Article
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  7. Non-coding RNA crosstalk with nuclear receptors in liver disease.Biochimica et biophysica acta. Molecular basis of disease · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The Circular RNA circSKA3 Binds Integrin β1 to Induce Invadopodium Formation Enhancing Breast Cancer Invasion.Molecular therapy : the journal of the American Society of Gene Therapy · 2020
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

11 authors at 8 institutions in 2 countries.

William W DuSunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
Fengqiong LiuSunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada; School of Public Health, Sun Yat-sen University, Guangzhou, P.R. China.
Sze Wan ShanSunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
Xindi Cindy MaSunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
Shaan GuptaSunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
Tianru JinToronto General Research Institute, University Health Network, Toronto, Ontario, Canada.
David SpanerSunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada.
Sergey N KrylovDepartment of Chemistry and Centre for Research on Biomolecular Interactions, York University, Toronto, Ontario, Canada.
Yaou ZhangKey Lab in Healthy Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, P.R. China.
Wenhua LingSchool of Public Health, Sun Yat-sen University, Guangzhou, P.R. China.
Burton B YangSunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada. Electronic address: byang@sri.utoronto.ca.
Health Sciences Centre · CASunnybrook Research InstituteSun Yat-sen University · CNSunnybrook Health Science Centre · CATsinghua University · CNUniversity Health Network · CAUniversity of Toronto · CAYork University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Steatosis is a pivotal event in the initiation and progression of nonalcoholic fatty liver disease (NAFLD) which can be driven by peroxisome proliferator-activated receptor-α (PPAR-α) dysregulation. Through examining the effect of PPAR-α on fatty liver development, we found that PPAR-α is a target of miR-17-5p. Transgenic mice expressing miR-17 developed fatty liver and produced higher levels of triglyceride and cholesterol but lower levels of PPAR-α. Ectopic expression of miR-17 enhanced cellular steatosis. Gain-of-function and loss-of-function experiments confirmed PPAR-α as a target of miR-17-5p. On the other hand, PPAR-α bound to the promoter of miR-17 and promoted its expression. The feed-back loop between miR-17-5p and PPAR-α played a key role in the induction of steatosis and fatty liver development. Mice with high levels of miR-17-5p were sensitive to Dexamethasone-induced fatty liver formation. Inhibition of miR-17-5p suppressed this process and enhanced PPAR-α expression in mice treated with Dexamethasone. Clofibrate, Ciprofibrate, and WY-14643: three agents used for treatment of metabolic disorders, were found to promote PPAR-α expression while decreasing miR-17-5p levels and inhibiting steatosis. Our studies show that miR-17-5p inhibitor and agents used in metabolic disorders may be applied in combination with Dexamethasone in the treatment of anti-inflammation, immunosuppression, and cancer patients.

Indexed as

AnimalsCholesterolDexamethasoneDisease Models, AnimalFatty LiverHumansLiverMiceMice, TransgenicMicroRNAsPPAR alphaTriglyceridesCholesterolDexamethasoneMicroRNAsMirn17 microRNA, mousePPAR alphaTriglycerides

Identifiers

PMID25896250
PMCPMC4817789
OpenAlexW2056327158

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.