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*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

6 Scopus citations


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.

Original languageEnglish
Article number2644
Issue number9
StatePublished - 01 05 2022

Bibliographical note

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© 2022 by the authors. Licensee MDPI, Basel, Switzerland.


  • DKK-1
  • KLF10
  • diabetes
  • renal fibrosis


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