Evidence mapPaperPMID 35565995Full record

ArticleMolecules (Basel, Switzerland)2022

Knockout of KLF10 Ameliorated Diabetic Renal Fibrosis via Downregulation of DKK-1.

Yung-Chien Hsu, Cheng Ho, Ya-Hsueh Shih, Wen-Chiu Ni, Yi-Chen Li, Hsiu-Ching Chang, Chun-Liang Lin

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. New Insights into the Role of KLF10 in Tissue Fibrosis.International journal of molecular sciences · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Therapeutic Potential of Extracts fromPlants (Basel, Switzerland) · 2023
    Article
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.

Yung-Chien HsuDepartment of Nephrology, Chang Gung Memorial Hospital, Chiayi 613, Taiwan.
Cheng HoKidney and Diabetic Complications Research Team (KDCRT), Chang Gung Memorial Hospital, Chiayi 613, Taiwan.
Ya-Hsueh ShihDepartment of Nephrology, Chang Gung Memorial Hospital, Chiayi 613, Taiwan.
Wen-Chiu NiDepartment of Nephrology, Chang Gung Memorial Hospital, Chiayi 613, Taiwan.
Yi-Chen LiDepartment of Nephrology, Chang Gung Memorial Hospital, Chiayi 613, Taiwan.
Hsiu-Ching ChangDepartment of Nephrology, Chang Gung Memorial Hospital, Chiayi 613, Taiwan.
Chun-Liang LinDepartment of Nephrology, Chang Gung Memorial Hospital, Chiayi 613, Taiwan.
Chiayi Chang Gung Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes-induced chronic kidney disease leads to mortality and morbidity and thus poses a great health burden worldwide. Krüppel-like factor 10 (KLF10), a zinc finger-containing transcription factor, regulates numerous cellular functions, such as proliferation, differentiation, and apoptosis. In this study, we explored the effects of KLF10 on diabetes-induced renal disease by using a KLF10 knockout mice model. Knockout of KLF10 obviously diminished diabetes-induced tumor growth factor-β (TGF-β), fibronectin, and type IV collagen expression, as evidenced by immunohistochemical staining. KLF10 knockout also repressed the expression of Dickkopf-1 (DKK-1) and phosphorylated β-catenin in diabetic mice, as evidenced by immunohistochemical staining and Western blot analysis. Quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) revealed that significantly decreased type IV collagen, fibronectin, and DKK-1 existed in KLF10 knockout diabetic mice compared with control diabetic mice. Moreover, knockout of KLF10 reduced the renal fibrosis, as shown by Masson's Trichrome analysis. Overall, the results indicate that depletion of KLF10 ameliorated diabetic renal fibrosis via the downregulation of DKK-1 expression and inhibited TGF-β1 and phosphorylated β-catenin expression. Our findings suggest that KLF10 may be a promising therapeutic choice for the treatment of diabetes-induced renal fibrosis.

Indexed as

Diabetes Mellitus, ExperimentalDiabetic NephropathiesKruppel-Like Transcription FactorsAnimalsbeta CateninCollagen Type IVDown-RegulationEarly Growth Response Transcription FactorsFemaleFibronectinsFibrosisHumansMaleMiceMice, KnockoutTransforming Growth Factor beta1beta CateninCollagen Type IVEarly Growth Response Transcription FactorsFibronectinsKLF10 protein, mouseKruppel-Like Transcription FactorsTransforming Growth Factor beta1diabetesDKK-1KLF10renal fibrosis

Identifiers

PMID35565995
PMCPMC9105565
OpenAlexW4224245868

What Socratic 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 Socratic graph.