ArticleScientific reports2016
Simultaneous deactivation of FAK and Src improves the pathology of hypertrophic scar.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
- Ranitidine attenuates myocardial fibrosis by suppressing histamine/H2 receptor signaling and FAK/Src activation.Frontiers in pharmacology · 2026Article
- Fast-Dissolving Sodium Alginate-Based Microneedle Patch Integrating Tranilast and Glabridin-Loaded Nanoparticles for Dual-Action Hypertrophic Scar Therapy.Biomaterials research · 2026Article
- Current therapeutic strategies and available research models for investigating hypertrophic scars.Frontiers in pharmacology · 2026Review
- Mechanical Signaling: Molecular Mechanisms, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2025Review
- The Promoting Effect of Animal Bioactive Proteins and Peptide Components on Wound Healing: A Review.International journal of molecular sciences · 2024Review
- Pharmacotherapy for Keloids and Hypertrophic Scars.International journal of molecular sciences · 2024Review
- Natural Polymeric Hydrogels Encapsulating Small Molecules for Diabetic Wound Healing.Gels (Basel, Switzerland) · 2023Review
- Metal Nanoparticle-Flavonoid Connections: Synthesis, Physicochemical and Biological Properties, as Well as Potential Applications in Medicine.Nanomaterials (Basel, Switzerland) · 2023Review
- Flavonoids as Potential Wound-Healing Molecules: Emphasis on Pathways Perspective.International journal of molecular sciences · 2023Review
- Mechanotransduction in skin wound healing and scar formation: Potential therapeutic targets for controlling hypertrophic scarring.Frontiers in immunology · 2022Review
- Article
- FAK Inhibition Attenuates Corneal Fibroblast Differentiation In Vitro.Biomolecules · 2021Article
- Review
- FAK Shutdown: Consequences on Epithelial Morphogenesis and Biomarker Expression Involving an Innovative Biomaterial for Tissue Regeneration.International journal of molecular sciences · 2021Article
- Leveraging Mechanical Forces to Target Insulin Injection-Induced Lipohypertrophy and Fibrosis.Diabetes spectrum : a publication of the American Diabetes Association · 2021Article
- Mechanotransduction in Wound Healing and Fibrosis.Journal of clinical medicine · 2020Review
- Article
- Article
- Interaction of Src and Alpha-V Integrin Regulates Fibroblast Migration and Modulates Lung Fibrosis in A Preclinical Model of Lung Fibrosis.Scientific reports · 2017Article
- Grafting both acute wound site and adjacent donor site with the same graft: an easy and safe procedure to improve healing and minimize pain in elderly and bedridden patients.Annals of burns and fire disasters · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertrophic scar (HS) is a serious fibrotic skin condition with currently no satisfactory therapy due to undefined molecular mechanism. FAK and Src are two important non-receptor tyrosine kinases that have been indicated in HS pathogenesis. Here we found both FAK and Src were activated in HS vs. normal skin (NS), NS fibroblasts treated with TGF-β1 also exhibited FAK/Src activation. Co-immunoprecipitation and dual-labelled immunofluorescence revealed an enhanced FAK-Src association and co-localization in HS vs. NS. To examine effects of FAK/Src activation and their interplay on HS pathogenesis, site-directed mutagenesis followed by gene overexpression was conducted. Results showed only simultaneous overexpression of non-phosphorylatable mutant FAK Y407F and phosphomimetic mutant Src Y529E remarkably down-regulated the expression of Col I, Col III and α-SMA in cultured HS fibroblasts, alleviated extracellular matrix deposition and made collagen fibers more orderly in HS tissue vs. the effect from single transfection with wild-type or mutational FAK/Src. Glabridin, a chemical found to block FAK-Src complex formation in cancers, exhibited therapeutic effects on HS pathology probably through co-deactivation of FAK/Src which further resulted in FAK-Src de-association. This study suggests FAK-Src complex could serve as a potential molecular target, and FAK/Src double deactivation might be a novel strategy for HS therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.