Source comparison
Research Design Comparison
Primary mechanism G-actin sequestration → cell migration TGF-β1-Smad2/3 → collagen synthesis Migration effect +38-52% scratch closure (HaCaT) +8-12% NS (fibroblast) Angiogenesis VEGF +28-34%, CD31+ +28-38% HIF-1α stabilisation (diabetic context) Collagen outpu
This comparison does not assign a generated winner or score.
- Primary mechanism
- G-actin sequestration → cell migration
- TGF-β1-Smad2/3 → collagen synthesis
- Migration effect
- +38-52% scratch closure (HaCaT)
- +8-12% NS (fibroblast)
- Angiogenesis
- VEGF +28-34%, CD31+ +28-38%
- HIF-1α stabilisation (diabetic context)
- Collagen output
- MMP-2 matrix clearing (migration support)
- Sircol +35-55%, PIP ELISA +38-52%
- Optimal wound phase
- Inflammation → early proliferation (day 0-7)
- Proliferation → remodelling (day 3-21)
- Ischaemic wound advantage
- VEGF-driven angiogenesis 2.4× closure
- Nrf2-HIF-1α ROS mitigation
- Key controls
- Cytochalasin D (actin), anti-TB-500 Ab
- SB431542 (ALK5/Smad), ML385 (Nrf2)
- 🇬🇧 UK Research Peptides: PeptidesLab UK supplies COA-verified TB-500 and GHK-Cu for research and laboratory use. View UK stock →