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Updated: Feb 9, 2026

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue
Published on: July 28, 2023
Downregulation of miR‑637 promotes proliferation and metastasis by targeting Smad3 in keloids
Ye Zhang1, Bingyu Guo1, Qiang Hui1
1Department of Reconstructive and Plastic Surgery, The General Hospital of Shenyang Military Region, Shenyang, Liaoning 110016, P.R. China.
Abstract:
Keloids are a type of abnormal scar tissue. MicroRNAs (miRNAs) exhibit a pivotal role in the regulation of cell proliferation and metastasis of keloids. miRNA microarray revealed that miR‑637 was one of the most frequently altered miRNAs in keloids. Furthermore, up-regulation of miR‑637 inhibited cell proliferation and metastasis by targeting mothers against decapentaplegic homolog (Smad)3, one of the important proteins that affects the formation of keloids. Further studies demonstrated that miR‑637 regulated the proliferation and metastasis of human keloid fibroblast (HKF) cells by mediating the Smad3 signaling pathway. Overall, the present findings suggest that miR‑637 may be a promising therapeutic target in keloids.
Insights
MicroRNAs (miRNAs) regulate keloid scarring. Increased miR-637 levels inhibit keloid cell proliferation and metastasis by targeting Smad3, suggesting miR-637 as a potential therapeutic target for abnormal scarring.
Area of Science:
- Dermatology
- Molecular Biology
- Biochemistry
Background:
- Keloids are abnormal scars resulting from dysregulated wound healing.
- MicroRNAs (miRNAs) are key regulators of cellular processes, including proliferation and metastasis.
- Altered miRNA expression is implicated in keloid pathogenesis.
Purpose of the Study:
- To investigate the role of specific microRNAs in keloid formation.
- To identify novel therapeutic targets for keloid treatment.
Main Methods:
- miRNA microarray analysis to identify differentially expressed miRNAs in keloids.
- In vitro studies using human keloid fibroblast (HKF) cells.
- Target validation by assessing the effect of miR-637 on Smad3 expression and signaling.
Main Results:
- miR-637 was identified as a significantly altered miRNA in keloids.
- Overexpression of miR-637 suppressed proliferation and metastasis of HKF cells.
- miR-637 directly targeted mothers against decapentaplegic homolog (Smad)3, inhibiting the Smad3 signaling pathway.
Conclusions:
- miR-637 plays a crucial role in regulating keloid fibroblast behavior.
- The miR-637/Smad3 axis is a key pathway in keloid development.
- miR-637 represents a potential therapeutic target for managing keloids.
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