From stem cells to skin: ADSCP6 peptide's role in transforming scar therapy.
Li J., Zeng S., Zhou B., Yan Q., Sun Y., Chen L.
Animal Study on Chronic Wound, Scar, published in Biochem Pharmacol (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Biochem Pharmacol (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40348095
- DOI
- 10.1016/j.bcp.2025.116980
Abstract (original English)
Hypertrophic scars, caused by abnormal wound healing after injury, involve excessive fibroblast activity, ECM dysregulation, and inflammation. Bioactive peptides show antifibrotic potential. Based on our previous discovery of scar-modulating peptides from adipose-derived stem cells, this study reveals how ADSCP6 (Adipose-derived stem cell peptide 6) suppresses hypertrophic scarring. In vitro analyses revealed that ADSCP6 significantly downregulated type I collagen and ACTA2 (alpha smooth muscle actin) expression in human hypertrophic scar fibroblasts (HSFs), without altering proliferative/apoptotic activity. In vivo, topical ADSCP6 administration enhanced wound healing and attenuated collagen content in a murine excisional wound model. Transcriptomic profiling (RNA-seq) identified 328 differentially expressed genes (182 upregulated, 146 downregulated) post-treatment, with KEGG (kyoto encyclopedia of genes and genomes) pathway enrichment implicating NF-κB (nuclear factor kappa-B) signaling as a primary mechanism. Protein interaction assays (pull-down/cellular thermal shift assays) identified KANK2 (KN motif and ankyrin repeat domains 2) and ADGRE2/EMR2 (adhesion G protein-coupled receptor E2) as ADSCP6-binding partners, while western blot confirmed NF-κB1 (p50) upregulation. Functional validation demonstrated that NF-κB pathway blockade abrogated ADSCP6's antifibrotic effects. A
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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