ArticleThe American journal of pathology2011
Temporal smad7 transgene induction in mouse epidermis accelerates skin wound healing.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- Integrative transcriptomic and machine learning analysis identifies candidate biomarkers and immune features in diabetic ulcers.Molecular biology reports · 2026Article
- Smad7-based biologic targeting epidermis and stroma promotes healing of diabetic wounds in mice and pigs.Nature communications · 2026Article
- The Phytochemical Composition and Molecular Mechanisms Involved in the Wound Healing Attributes ofPlants (Basel, Switzerland) · 2025Review
- TriHex 2.0-Advancing Skin Health Science and the TriHex Technology.Journal of cosmetic dermatology · 2025Article
- Metabolism-related biomarkers, molecular classification, and immune infiltration in diabetic ulcers with validation.International wound journal · 2023Article
- Understanding Transcriptional Networks Regulating Initiation of Cutaneous Wound Healing.The Yale journal of biology and medicine · 2020Review
- Smad7 Ameliorates TGF-β-Mediated Skin Inflammation and Associated Wound Healing Defects but Not Susceptibility to Experimental Skin Carcinogenesis.The Journal of investigative dermatology · 2019Article
- Sheng-ji Hua-yu formula promotes diabetic wound healing of re-epithelization via Activin/Follistatin regulation.BMC complementary and alternative medicine · 2018Article
- Topical Application of Tat-Rac1 Promotes Cutaneous Wound Healing in Normal and Diabetic Mice.International journal of biological sciences · 2018Article
- 20(S)-Protopanaxadiol enhances angiogenesis via HIF-1α-mediated VEGF secretion by activating p70S6 kinase and benefits wound healing in genetically diabetic mice.Experimental & molecular medicine · 2017Article
- Regulation of TGF-β Family Signaling by Inhibitory Smads.Cold Spring Harbor perspectives in biology · 2017Review
- Transition from inflammation to proliferation: a critical step during wound healing.Cellular and molecular life sciences : CMLS · 2016Review
- Re-epithelialization of cutaneous wounds in adult zebrafish combines mechanisms of wound closure in embryonic and adult mammals.Development (Cambridge, England) · 2016Article
- The role of Smad7 in oral mucositis.Protein & cell · 2015Review
- Smad7 enhances ATM activity by facilitating the interaction between ATM and Mre11-Rad50-Nbs1 complex in DNA double-strand break repair.Cellular and molecular life sciences : CMLS · 2015Article
- The Role of TGFβ Signaling in Wound Epithelialization.Advances in wound care · 2014Review
- CtBP1 overexpression in keratinocytes perturbs skin homeostasis.The Journal of investigative dermatology · 2014Article
- Galvanic microparticles increase migration of human dermal fibroblasts in a wound-healing model via reactive oxygen species pathway.Experimental cell research · 2014Article
- Knockout of endothelial cell-derived endothelin-1 attenuates skin fibrosis but accelerates cutaneous wound healing.PloS one · 2014Article
- Effects and mechanisms of a microcurrent dressing on skin wound healing: a review.Military Medical Research · 2014Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
The expression of Smad7, a tumor growth factor-β (TGFβ) antagonist, is increased during cutaneous wound healing. To assess this significance, we temporally induced Smad7 transgene expression in wounded skin in gene-switch-Smad7 transgenic (Smad7 tg) mice. Smad7 induction in epidermal keratinocytes caused an increase in keratinocyte proliferation with reduced Smad2 activation, indicating that Smad7 abrogated TGFβ-mediated growth inhibition. Additionally, wounded skin from Smad7 tg mice exhibited accelerated re-epithelialization, with increased activation of extracellular signal-regulated kinase (Erk), and an in vitro migration assay revealed that Erk activation contributed to Smad7-mediated keratinocyte migration. Notably, epidermis-specific Smad7 transgene expression also has a profound effect on the wound stroma, resulting in reduced inflammation, angiogenesis, and production of type I collagen. Reduced Smad2 activation was observed in wounded stroma from Smad7 transgenic (Smad7 tg) mice, possibly owing to fewer infiltrated TGFβ-producing leukocytes compared to those in wounds from control mice. Because Smad7 is not secreted, these effects could reflect functional changes in Smad7 tg keratinocytes. Supporting this notion, the activation of NF-κB, a nonsecreted protein complex that transcriptionally activates inflammatory cytokines, was reduced in wounded epidermis from Smad7 tg mice compared to that in wounded wild-type epidermis. In sum, epidermal Smad7 overexpression accelerated wound healing through its direct effects on keratinocyte proliferation and migration, and through indirect effects on wound stroma.
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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.