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Updated: Jun 26, 2025

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Angiotensin (1-7) Inhibits Transforming Growth Factor-Β1-Induced Epithelial-Mesenchymal Transition of Human

Yueda Jihu1,2, Ruobing Leng1, Mengchang Liu1,2

  • 1Clinical College of Medicine, Southwest Medical University, Lu zhou, People's Republic of China.

Clinical, Cosmetic and Investigational Dermatology
|May 13, 2024
PubMed
Abstract

Insights

Angiotensin (1-7) inhibits TGF-β1-induced skin cell changes by blocking key signaling pathways. This finding offers potential new treatments for fibrotic skin conditions like keloids.

Area of Science:

  • Cell Biology
  • Dermatology
  • Endocrinology

Background:

  • Epithelial-mesenchymal transition (EMT) is implicated in skin fibrotic diseases.
  • Angiotensin (1-7) (Ang-(1-7)) is a peptide hormone with known anti-fibrosis effects.
  • The role of Ang-(1-7) in skin EMT remains largely unexplored.

Purpose of the Study:

  • To investigate the effect of Ang-(1-7) on Transforming growth factor-β1 (TGF-β1)-induced EMT in human keratinocytes (HaCaT cells) in vitro.

Main Methods:

  • Utilized HaCaT cells treated with TGF-β1 and/or Ang-(1-7).
  • Assessed cell proliferation (CCK-8), migration (scratch assay), and protein expression (Western blotting).
  • Analyzed EMT-related gene expression using quantitative real-time PCR.

Main Results:

  • Ang-(1-7) reduced TGF-β1-induced HaCaT cell migration.
  • Ang-(1-7) decreased expression of α-SMA and vimentin, while restoring E-cadherin and claudin-1.
  • Ang-(1-7) inhibited Smad2/3 phosphorylation and suppressed EMT-transcription factors (SNAI2, TWIST1, ZEB1).

Conclusions:

  • Ang-(1-7) effectively inhibits TGF-β1-induced EMT in HaCaT cells.
  • The mechanism involves disruption of the TGF-β1-Smad canonical signaling pathway.
  • These findings suggest Ang-(1-7) as a potential therapeutic agent for keloids and other fibrotic skin diseases.
Keywords:
angiotensin (1-7)epithelial-mesenchymal transitionkeratinocytestransforming growth factor-β

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