Related Experiment Video

Updated: Jan 7, 2026

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue
04:41

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue

Published on: July 28, 2023

3.3K

KLF2 inhibits keloid progression by targeting PI3K/AKT-mediated MMP-2/9 signaling

Dan Yu1, AoLin Zhao2, ZhiGuo Wang2

  • 1Department of Pathology, Taihe Hospital, Hubei University of Medicine, Shiyan City, 442000 Hubei Province China.

Cytotechnology
|December 26, 2025
PubMed

Insights

Krüppel-like factor 2 (KLF2) inhibits keloid fibroblast proliferation and migration. Upregulating KLF2 may offer new therapeutic strategies for keloid disorder by targeting the PI3K/AKT pathway.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Cell Biology

Background:

  • Keloid disorder (KD) is characterized by excessive fibroblast proliferation, migration, and invasion.
  • The role of Krüppel-like factor 2 (KLF2) in the pathogenesis of keloids and hypertrophic scars is not fully understood.

Purpose of the Study:

  • To investigate the anti-proliferation, anti-invasion, and anti-migration activities of KLF2 in keloid fibroblasts (KFs) and hypertrophic scar fibroblasts (HSFs).
  • To elucidate the molecular pathways involved in KLF2's function in keloid pathogenesis.

Main Methods:

  • Quantification of KLF2 expression in normal skin, keloid, and hypertrophic scar tissues and cell lines using western blot and qRT-PCR.
  • Assessment of fibroblast proliferation, migration, and invasion.
  • Western blot analysis to identify key pathway proteins.

Main Results:

  • KLF2 expression was significantly lower in keloid and hypertrophic scar tissues compared to normal skin.
  • Overexpression of KLF2 inhibited proliferation, migration, and invasion in both KFs and HSFs.
  • KLF2 overexpression downregulated MMP-2, MMP-9, PI3K, and p-Akt in KFs, and PI3K/AKT pathway proteins in HSFs.

Conclusions:

  • KLF2 inhibits keloid fibroblast proliferation and migration by downregulating MMP-2/9 via the PI3K/AKT pathway.
  • KLF2 represents a potential therapeutic target for keloid disorder.
  • These findings provide novel insights into KLF2's function and molecular mechanisms in keloid pathogenesis, suggesting new clinical treatment strategies.
Keywords:
KLF2KeloidMMP-2MMP-9PI3K/Akt signaling

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