Evidence map›Paper›PMID 40497041›Full record

ArticleCytotechnology2025

Effect of miR-29a-3p on renal interstitial fibrosis in diabetic kidney disease through FOXP1-mediated TGF-β1/Smad3 signaling pathway.

Juntai Zhang, Yan Qin, Jie Liu, Jie Ding, Mengying Xu, Li Yang, Yuanxin Zheng, Chin Kai Ling, Xi Zhang

Abstract read
In one paragraph

Article in Cytotechnology, 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. miRNA in the Progression of Diabetic Kidney Disease: New Insight.International journal of molecular sciences · 2025
    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

9 authors.

Juntai ZhangFaculty of Medicine and Health Science, University Malaysia Sabah, 88400 Kota Kinabalu, Sabah Malaysia.
Yan QinDepartment of Nephrology & Immunology, Affiliated Ganmei Hospital of Kunming Medical University, Kunming, 650224 Yunnan China.
Jie LiuDepartment of Pathology, Affiliated Ganmei Hospital of Kunming Medical University, Kunming, 650224 Yunnan China.
Jie DingDepartment of Ultrasound, Affiliated Ganmei Hospital of Kunming Medical University, Kunming, 650224 Yunnan China.
Mengying XuDepartment of Nephrology & Immunology, Affiliated Ganmei Hospital of Kunming Medical University, Kunming, 650224 Yunnan China.
Li YangDepartment of Nephrology & Immunology, Affiliated Ganmei Hospital of Kunming Medical University, Kunming, 650224 Yunnan China.
Yuanxin ZhengDepartment of Nephrology & Immunology, Affiliated Ganmei Hospital of Kunming Medical University, Kunming, 650224 Yunnan China.
Chin Kai LingFaculty of Medicine and Health Science, University Malaysia Sabah, 88400 Kota Kinabalu, Sabah Malaysia.
Xi ZhangDepartment of Nephrology & Immunology, Affiliated Ganmei Hospital of Kunming Medical University, Kunming, 650224 Yunnan China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal interstitial fibrosis (RIF) is a major manifestation of diabetic kidney disease (DKD). This study aimed to elucidate the specific mechanism by which miR-29a-3p affects RIF in DKD through Forkhead box protein 1 (FOXP1)-mediated TGF-β1/Smad3 and to provide novel ideas and therapeutic targets for RIF. Cell and animal models were constructed, and CCK-8, flow cytometry, Western blotting, immunofluorescence, RT‒qPCR, Masson's trichrome staining, hematoxylin-eosin (HE) and periodic acid-Schiff (PAS) staining, Sirius red staining, and immunohistochemistry were used to detect the related indicators of RIF in DKD. The interaction between miR-29a-3p and FOXP1 was confirmed using a dual-luciferase assay. These findings suggested that miR-29a-3p can act on renal interstitial fibrosis cells in DKD through the TGF-β1/Smad3 signaling pathway mediated by FOXP1. The overexpression of miR-29a-3p inhibited the expression of fibrin-associated proteins in renal tissue, contracted the mesangial matrix and decreased the accumulation of renal fibrils to ultimately alleviate RIF in DKD. This study is the first to propose the specific molecular mechanism of miR-29a-3p in renal interstitial cells in DKD, which provides novel targets and strategies for the clinical treatment of RIF-related DKD. Graphical Abstract:

Indexed as

Diabetic kidney diseaseFOXP1miR-29a-3pRenal interstitial fibrosisTGF-β1/Smad3

Identifiers

PMID40497041
PMCPMC12146237

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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.