Evidence map›Paper›PMID 24694752›Full record

ArticleScientific reports2014

miR-34c attenuates epithelial-mesenchymal transition and kidney fibrosis with ureteral obstruction.

Ryuji Morizane, Shizuka Fujii, Toshiaki Monkawa, Ken Hiratsuka, Shintaro Yamaguchi, Koichiro Homma, Hiroshi Itoh

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. miR-122-5p Regulates Renal Fibrosis In Vivo.International journal of molecular sciences · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Down-regulation of LINC00667 hinders renal tubular epithelial cell apoptosis and fibrosis through miR-34c.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
  13. Epigenetics in kidney diseases.Advances in clinical chemistry · 2021
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Urinary microRNA in kidney disease: utility and roles.American journal of physiology. Renal physiology · 2019
    Review
  20. Non-Coding RNAs as New Therapeutic Targets in the Context of Renal Fibrosis.International journal of molecular sciences · 2019
    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

7 authors at 1 institution in 1 country.

Ryuji Morizane1] Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan [2].
Shizuka Fujii1] Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan [2].
Toshiaki MonkawaDepartment of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Ken HiratsukaDepartment of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Shintaro YamaguchiDepartment of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Koichiro HommaDepartment of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Hiroshi ItohDepartment of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Keio University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

micro RNAs (miRNAs) are small non-coding RNAs that act as posttranscriptional repressors by binding to the 3'-UTR of target mRNAs. On the other hand, mesenchymal-epithelial transition (EMT) and kidney fibrosis is a pathological process of chronic kidney disease (CKD), and its relationship to miRNAs is becoming recognized as a potential target for CKD therapies. To find new miRNAs involved in EMT, we examined miRNA expression in experimental models of EMT and renal epithelialization using microarray, and found that miR-34c attenuates EMT induced by TGF-β in a mouse tubular cell line. To confirm the effects of miR-34c in vivo, we administered the precursor of miR-34c to mice with unilateral ureteral obstruction, and miR-34c decreased kidney fibrosis area and the expression of connective tissue growth factor, α-SMA, collagen type 1, collagen type 3 and fibronectin. In conclusion, our study showed miR-34c attenuates EMT and kidney fibrosis of mice with ureteral obstruction.

Indexed as

Epithelial-Mesenchymal TransitionActinsAnimalsCalcium-Binding ProteinsCell LineCollagen Type ICollagen Type IIIConnective Tissue Growth FactorFibronectinsFibrosisIntercellular Signaling Peptides and ProteinsKidneyMembrane ProteinsMiceMicroRNAsOligonucleotides, AntisenseActa2 protein, mouseActinsCalcium-Binding ProteinsCollagen Type ICollagen Type IIIConnective Tissue Growth FactorFibronectinsIntercellular Signaling Peptides and ProteinsMembrane ProteinsMicroRNAsOligonucleotides, AntisenseSerrate-Jagged ProteinsTransforming Growth Factor beta

Identifiers

PMID24694752
PMCPMC3974136
OpenAlexW2043373020

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.