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2000
Volume 25, Issue 10
  • ISSN: 1566-5240
  • E-ISSN: 1875-5666

Abstract

Background

Keloid formation is characterized by excessive production of extracellular matrix, leading to dysregulated fibroproliferative collagen response. N6-methyl-adenosine (m6A) modification plays an essential role in this process.

Objective

Our objective in this study was to explore the mechanism of m6A methyltransferase KIAA1429 in keloid formation.

Methods

We examined the impact of m6A methyltransferase KIAA1429 on keloid formation using qRT-PCR, Western blot, immunofluorescence, Transwell migration assay, and MeRIP-qPCR.

Results

KIAA1429 was downregulated in keloid tissue. Overexpression of KIAA1429 suppressed fibroblast migration and reduced COL1A1 and α-SMA levels. Conversely, the knockdown of KIAA1429 promoted fibroblast migration and COL1A1 and α-SMA levels. Additionally, overexpression of KIAA1429 inhibited the TGF-β1/Smad pathway. Mechanistic experiments suggested that KIAA1429 regulated TGF-β1 m6A modification, maintained TGF-β1 mRNA stability, and participated in the regulation of keloid formation. Furthermore, TGF-β1 could reverse the effects of KIAA1429 overexpression on fibroblast migration and collagen deposition.

Conclusion

Taken together, our study suggested that KIAA1429 promoted keloid formation through the TGF-β1/Smad pathway, providing new insights for the treatment of keloid.

© 2025 Bentham Science Publishers
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2024-11-07
2025-12-13

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/content/journals/cmm/10.2174/0115665240307157241104095116
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KIAA1429 Promotes Keloid Formation Through the TGF-Β1/Smad Pathway
Current Molecular Medicine 25, 1290 (2025); https://doi.org/10.2174/0115665240307157241104095116
/content/journals/cmm/10.2174/0115665240307157241104095116
/content/journals/cmm/10.2174/0115665240307157241104095116
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  • Article Type:     Research Article
Keyword(s): keloid; KIAA1429; m6A; pathway; Smad; TGF-β1

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