Evidence map›Paper›PMID 41323794›Full record

ArticleMolecular therapy. Nucleic acids2025

Systemic miR-26a deficiency attenuates pulmonary fibrosis via PTEN upregulation and downstream TIMP-1 suppression.

Arisa Hamada, Kiyofumi Shimoji, Taku Nakashima, Kakuhiro Yamaguchi, Shinjiro Sakamoto, Yasushi Horimasu, Takeshi Masuda, Hiroshi Iwamoto, Hironobu Hamada, Yun Guo and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular therapy. Nucleic acids, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

13 authors.

Arisa HamadaDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Kiyofumi ShimojiDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Taku NakashimaDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Kakuhiro YamaguchiDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Shinjiro SakamotoDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yasushi HorimasuDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Takeshi MasudaDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Hiroshi IwamotoDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Hironobu HamadaDepartment of Physical Analysis and Therapeutic Sciences, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yun GuoDepartment of Immunology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Tomoharu YasudaDepartment of Immunology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Shigeru MiyakiDepartment of Orthopedic Surgery, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Noboru HattoriDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several microRNAs (miRNAs) have been implicated in the pathophysiology of pulmonary fibrosis; however, the detailed mechanisms remain unclear. miR-26a has demonstrated antifibrotic effects, particularly when its expression is suppressed in the airways. However, the effects of systemic miR-26a deficiency on pulmonary fibrosis have not been investigated. We found that miR-26a knockout (KO) mice exhibited reduced pulmonary fibrosis compared with wild-type (WT) mice. Whole-lung RNA sequencing analysis indicated that the mammalian target of rapamycin complex 1 (MTORC1) signaling and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathways were elevated in the WT group compared with the KO group. Loss of miR-26a increases

Indexed as

microRNAmiR-26aMT: Non-coding RNAsPTENpulmonary fibrosisTIMP-1

Identifiers

PMID41323794
PMCPMC12663618

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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.