Evidence map›Paper›PMID 36808381›Full record

ArticleClinical and experimental nephrology2023

MiR-34a induces myofibroblast differentiation from renal fibroblasts.

Suguru Saito, Shin-Ichiro Ohno, Yuichirou Harada, Yoshihiko Kanno, Masahiko Kuroda

Abstract read
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In one paragraph

Article in Clinical and experimental nephrology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Nintedanib Attenuates Epidural Fibrosis after Laminectomy in Rats.Journal of Korean Neurosurgical Society · 2026
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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

5 authors at 1 institution in 1 country.

Suguru SaitoDepartment of Nephrology, Tokyo Medical University, Tokyo, Japan.
Shin-Ichiro OhnoDeparatment of Molecular Pathology, Tokyo Medical University, 6-1-1, Shinjuku, Shinjuku-ku, Tokyo, 160-8402, Japan. s-ohno@tokyo-med.ac.jp.ORCID http://orcid.org/0000-0003-1064-4750
Yuichirou HaradaDeparatment of Molecular Pathology, Tokyo Medical University, 6-1-1, Shinjuku, Shinjuku-ku, Tokyo, 160-8402, Japan.
Yoshihiko KannoDepartment of Nephrology, Tokyo Medical University, Tokyo, Japan.
Masahiko KurodaDeparatment of Molecular Pathology, Tokyo Medical University, 6-1-1, Shinjuku, Shinjuku-ku, Tokyo, 160-8402, Japan.
Tokyo Medical University · JP

Funding

Japan Society for the Promotion of Science KAKENHI 17K16101Japan Society for the Promotion of Science KAKENHI 21K06953
6 · The paper itself

Abstract

backgroundRenal fibrosis is the common outcome of progressive kidney diseases. To avoid dialysis, the molecular mechanism of renal fibrosis must be explored further. MicroRNAs play key roles in renal fibrosis. MiR-34a is a transcriptional target of p53, which regulates the cell cycle and apoptosis. Previous studies demonstrated that miR-34a promotes renal fibrosis. However, the distinct roles of miR-34a in renal fibrosis have not been fully elucidated. Here, we identified the roles of miR-34a in renal fibrosis.

methodWe first analyzed p53 and miR-34a expression in kidney tissues in s UUO (unilateral ureteral obstruction) mouse model. Then, to confirm the effects of miR-34a in vitro, we transfected a miR-34a mimic into a kidney fibroblast cell line (NRK-49F) and analyzed.

resultsWe found that the expression of p53 and miR-34a was upregulated after UUO. Furthermore, after transfection of the miR-34a mimic into kidney fibroblasts, the expression of α-SMA was upregulated dramatically. In addition, α-SMA upregulation was greater upon transfection of the miR-34a mimic than upon treatment with TGF-β1. Moreover, high expression of Acta2 was maintained despite sufficient removal of the miR-34a mimic by changing the medium 4 times during the 9-day culture. After transfection of the miR-34a mimic into kidney fibroblasts, we did not detect phospho-SMAD2/3 by immunoblotting analysis.

conclusionOur study revealed that miR-34a induces myofibroblast differentiation from renal fibroblasts. Moreover, the miR-34a-induced upregulation of α-SMA was independent of the TGF-β/SMAD signaling pathway. In conclusion, our study indicated that the p53/miR-34a axis promotes the development of renal fibrosis.

Indexed as

Cell DifferentiationKidney DiseasesMicroRNAsMyofibroblastsAnimalsFibroblastsFibrosisKidneyMiceRenal DialysisTransforming Growth Factor beta1Tumor Suppressor Protein p53Ureteral ObstructionMicroRNAsMIRN34a microRNA, mouseTransforming Growth Factor beta1Tumor Suppressor Protein p53miR-34aMyofibroblastRenal fibrosis

Identifiers

PMID36808381
OpenAlexW4321350900

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.