Evidence map›Paper›PMID 38745066›Full record

ArticleScientific reports2024

Inducible deletion of microRNA activity in kidney mesenchymal cells exacerbates renal fibrosis.

Hirofumi Sakuma, Keisuke Maruyama, Tatsuya Aonuma, Yuya Kobayashi, Taiki Hayasaka, Kohei Kano, Satoshi Kawaguchi, Kei-Ichi Nakajima, Jun-Ichi Kawabe, Naoyuki Hasebe and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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.

Hirofumi SakumaDivision of Cardiology and Nephrology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa, Japan.
Keisuke MaruyamaDivision of Cardiology and Nephrology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa, Japan.
Tatsuya AonumaDivision of Cardiology and Nephrology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa, Japan.
Yuya KobayashiDivision of Cardiology and Nephrology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa, Japan.
Taiki HayasakaDivision of Cardiology and Nephrology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa, Japan.
Kohei KanoDivision of Cardiology and Nephrology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa, Japan.
Satoshi KawaguchiDepartment of Emergency Medicine, Asahikawa Medical University, Asahikawa, Japan.
Kei-Ichi NakajimaDepartment of Biochemistry, Asahikawa Medical University, Asahikawa, Japan.
Jun-Ichi KawabeDepartment of Biochemistry, Asahikawa Medical University, Asahikawa, Japan.
Naoyuki HasebeDivision of Cardiology and Nephrology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa, Japan.
Naoki NakagawaDivision of Cardiology and Nephrology, Department of Internal Medicine, Asahikawa Medical University, Midorigaoka-Higashi 2-1-1-1, Asahikawa, Japan. naka-nao@asahikawa-med.ac.jp.

Funding

Japan Society for the Promotion of Science JP22K08300
6 · The paper itself

Abstract

MicroRNAs (miRNAs) are sequence-specific inhibitors of post-transcriptional gene expression. However, the physiological functions of these non-coding RNAs in renal interstitial mesenchymal cells remain unclear. To conclusively evaluate the role of miRNAs, we generated conditional knockout (cKO) mice with platelet-derived growth factor receptor-β (PDGFR-β)-specific inactivation of the key miRNA pathway gene Dicer. The cKO mice were subjected to unilateral ureteral ligation, and renal interstitial fibrosis was quantitatively evaluated using real-time polymerase chain reaction and immunofluorescence staining. Compared with control mice, cKO mice had exacerbated interstitial fibrosis exhibited by immunofluorescence staining and mRNA expression of PDGFR-β. A microarray analysis showed decreased expressions of miR-9-5p, miR-344g-3p, and miR-7074-3p in cKO mice compared with those in control mice, suggesting an association with the increased expression of PDGFR-β. An analysis of the signaling pathways showed that the major transcriptional changes in cKO mice were related to smooth muscle cell differentiation, regulation of DNA metabolic processes and the actin cytoskeleton, positive regulation of fibroblast proliferation and Ras protein signal transduction, and focal adhesion-PI3K/Akt/mTOR signaling pathways. Depletion of Dicer in mesenchymal cells may downregulate the signaling pathway related to miR-9-5p, miR-344g-3p, and miR-7074-3p, which can lead to the progression of chronic kidney disease. These findings highlight the possibility for future diagnostic or therapeutic developments for renal fibrosis using miR-9-5p, miR-344g-3p, and miR-7074-3p.

Indexed as

FibrosisKidneyMesenchymal Stem CellsMice, KnockoutMicroRNAsReceptor, Platelet-Derived Growth Factor betaRibonuclease IIIAnimalsDEAD-box RNA HelicasesKidney DiseasesMaleMiceSignal TransductionDEAD-box RNA HelicasesMicroRNAsReceptor, Platelet-Derived Growth Factor betaRibonuclease IIIDicermiR-9-5pmiRNAsRenal fibrosis

Identifiers

PMID38745066
PMCPMC11094108

What OpenQuestion holds

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Registered trials

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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.