ArticleTissue engineering and regenerative medicine2024
Zinc-Alpha-2-Glycoprotein Peptide Downregulates Type I and III Collagen Expression via Suppression of TGF-β and p-Smad 2/3 Pathway in Keloid Fibroblasts and Rat Incisional Model.
Article in Tissue engineering and regenerative medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Exploring the Complexities of TGF-β Signaling in Keloids: Beyond the Classical Smad Pathway.International journal of molecular sciences · 2026Review
- Exploration of novel therapeutic targets for keloids based on clinical and molecular data: the role of the IL-4/IL-13 signaling pathway.European journal of medical research · 2025Article
- Hypertrophic Scarring and Keloids: Epidemiology, Molecular Pathogenesis, and Therapeutic Interventions.MedComm · 2025Review
- Clinical Efficacy and Safety of Two Cycles of Intra-Articular Injection of Porcine Atelocollagen Versus Hyaluronic Acid in Knee Osteoarthritis.Bioengineering (Basel, Switzerland) · 2025Article
- Polynucleotide and Hyaluronic Acid Mixture for Skin Wound Dressing for Accelerated Wound Healing.Tissue engineering and regenerative medicine · 2025Article
- Cell-free adipose extract inhibits hypertrophic scar formation through collagen remodeling and antiangiogenesis.Open medicine (Warsaw, Poland) · 2025Article
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6 authors.
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Abstract
backgroundKeloids and hypertrophic scars result from abnormal collagen accumulation and the inhibition of its degradation. Although the pathogenesis remains unclear, excessive accumulation of the extracellular matrix (ECM) is believed to be associated with the TGF-β/SMAD pathway. Zinc-alpha-2-glycoprotein (ZAG) inhibits TGF-β-mediated epithelial-to-mesenchymal transdifferentiation and impacts skin barrier functions. In this study, we investigated the potential of a small ZAG-derived peptide against hypertrophic scars and keloids.
methodsThe study examined cell proliferation and mRNA expression of collagen types I and III in human dermal fibroblast (HDF) cell lines and keloid-derived fibroblasts (KF) following ZAG peptide treatment. A rat incisional wound model was used to evaluate the effect of ZAG peptide in scar tissue.
resultsSignificantly lower mRNA levels of collagen types I and III were observed in ZAG-treated fibroblasts, whereas matrix metalloproteinase (MMP)-1 and MMP-3 mRNA levels were significantly increased in HDFs and KFs. Furthermore, ZAG peptide significantly reduced protein expression of collagen type I and III, TGF-β1, and p-Smad2/3 complex in KFs. Rat incisional scar models treated with ZAG peptide presented narrower scar areas and reduced immature collagen deposition, along with decreased expression of collagen type I, α-SMA, and p-Smad2/3.
conclusionZAG peptide effectively suppresses the TGF-β and p-Smad2/3 pathway and inhibits excessive cell proliferation during scar formation, suggesting its potential therapeutic implications against keloids and hypertrophic scars.
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