ArticleMolecular medicine reports2020
Smad‑binding decoy reduces extracellular matrix expression in human hypertrophic scar fibroblasts.
Article in Molecular medicine reports, 2020. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed.
- Chirality-Dependent Supramolecular Biomaterials Remodeling of Scar Microenvironment via Integrin-Mediated Regulation for Hypertrophic Scars Therapy.Nano-micro letters · 2026Article
- Comparative Evaluation of Single and Combination Pharmacologic and Device-Based Anti-scar Therapies in a Murine Linear Wound Model.Aesthetic plastic surgery · 2026Article
- Myostatin in Obesity: A Molecular Link Between Metabolic Dysfunction and Musculotendinous Remodeling.International journal of molecular sciences · 2026Review
- Propolis compound inhibits profibrotic TGF-β1/SMAD signalling in human fibroblasts.Scientific reports · 2025Article
- Deciphering Collagen Phenotype Dynamics Regulators: Insights from In-Silico Analysis.Journal of bioinformatics and systems biology : Open access · 2024Article
- Transdermal delivery of Chinese herbal medicine extract using dissolvable microneedles for hypertrophic scar treatment.Acta pharmaceutica Sinica. B · 2021Article
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Authors and funding
5 authors.
Funding
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Abstract
The exact mechanisms underlying hypertrophic scarring is yet to be fully understood. However, excessive collagen deposition by fibroblasts has been demonstrated to result in hypertrophic scar formation, and collagen synthesis in dermal fibroblasts is regulated by the transforming growth factor‑β1/Smad signaling pathway. In view of this, a Smad‑binding decoy was designed and its effects on hypertrophic scar‑derived human skin fibroblasts was evaluated. The results of the present study revealed that the Smad decoy attenuates the total amount of collagen, collagen I and Smad2/3 expression in scar fibroblasts. Data from RNA sequencing indicated that the Smad decoy induced more than 4‑fold change in 178 genes, primarily associated with to the extracellular matrix, compared with the untreated control. In addition, results from quantitative real‑time polymerase chain reaction further confirmed that the Smad decoy significantly attenuated the expression of extracellular matrix‑related genes, including COL1A1, COL1A2 and COL3A1. Furthermore, the Smad decoy reduced transforming growth factor‑β1‑induced collagen deposition in scar fibroblasts. Data generated from the present study provide evidence supporting the use of the Smad decoy as a potential hypertrophic scar treatment.
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