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Related Concept Videos

TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...

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Related Experiment Video

Updated: Jun 17, 2026

A Mouse Model of Mechanotransduction-driven, Human-like Hypertrophic Scarring
05:54

A Mouse Model of Mechanotransduction-driven, Human-like Hypertrophic Scarring

Published on: November 29, 2024

Botulinum Toxin Type A Alleviates Hypertrophic Scar Formation in a Rabbit Ear Model by Inhibiting the TGF-β1/Smad

Yue-Hua Li1, Xiao-Wen Li2, Lei Ren2

  • 1Department of Geriatric General Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China. liyuehua@xjtu.edu.cn.

Aesthetic Plastic Surgery
|June 15, 2026
PubMed
Summary
This summary is machine-generated.

Botulinum toxin type A (BTA) and decorin reduce hypertrophic scarring by inhibiting key molecular pathways. This study elucidates BTA's mechanism in attenuating scar formation, offering potential new therapeutic strategies.

Keywords:
Animal modelBotulinum toxin type AHypertrophic scarTGF-β1

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Last Updated: Jun 17, 2026

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In Vitro Model of Human Cutaneous Hypertrophic Scarring using Macromolecular Crowding
08:20

In Vitro Model of Human Cutaneous Hypertrophic Scarring using Macromolecular Crowding

Published on: May 1, 2020

Area of Science:

  • Biomedical research
  • Dermatology
  • Wound healing research

Background:

  • Postoperative hypertrophic scarring is a common clinical issue with limited treatment options.
  • Botulinum toxin type A (BTA) has shown scar-inhibitory effects, but its molecular mechanisms are not fully understood.
  • Investigating BTA's role in scar reduction is crucial for developing effective therapies.

Purpose of the Study:

  • To explore the molecular pathways by which Botulinum toxin type A (BTA) attenuates hypertrophic scar formation.
  • To evaluate the efficacy of BTA and decorin in reducing scar height, collagen deposition, and TGF-β1 expression.
  • To elucidate the mechanism of BTA action in a rabbit auricular cicatricial model.

Main Methods:

  • Hypertrophic scar model established in 16 New Zealand white rabbits.
  • Interventions included BTA, decorin, or combined BTA and decorin injections; control received saline.
  • Scar height, collagen deposition, TGF-β1 levels, and protein expression (Smad2/3, MMP2, α-SMA, collagen I) were assessed.

Main Results:

  • All treatment groups showed reduced scar height, collagen deposition, and TGF-β1 expression compared to controls at 4 and 8 weeks.
  • BTA and/or decorin suppressed the Smad2/3 phosphorylation pathway.
  • MMP2 activity and protein expression of α-SMA and collagen I were reduced by BTA and/or decorin.

Conclusions:

  • Botulinum toxin type A (BTA) effectively improves scar appearance and reduces scar formation.
  • BTA inhibits the TGF-β1/Smad signaling pathway, leading to decreased collagen deposition.
  • These findings highlight BTA's potential as a therapeutic agent for hypertrophic scars.