ArticlePloS one2016
E2F1 Hinders Skin Wound Healing by Repressing Vascular Endothelial Growth Factor (VEGF) Expression, Neovascularization, and Macrophage Recruitment.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 16 citations in OpenAlex.
- Genetic variants of ACTC1 gene promoter in pediatric patients with sporadic patent ductus arteriosus and pathological significance.Pediatric research · 2026Article
- Article
- The use of occlusive dressings: influence on excisional wound healing in animal model.Acta cirurgica brasileira · 2023Article
- Exosomes Derived from E2F1International journal of nanomedicine · 2023Article
- An active ingredient isolated fromAging · 2022Article
- Fibroblast-like cells Promote Wound Healing via PD-L1-mediated Inflammation Resolution.International journal of biological sciences · 2022Article
- Knockout of E2F1 enhances the polarization of M2 phenotype macrophages to accelerate the wound healing process.The Kaohsiung journal of medical sciences · 2020Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundRefractory surface of wound and dermal chronic ulcer are largely attributed to poor neovascularization. We have previously shown that E2F1 suppresses VEGF expression in the ischemic heart, and that genetic deletion of E2F1 leads to better cardiac recovery. However, whether E2F1 has a role in dermal wound healing is currently not known. METHODS AND
resultsSkin wounds were surgically induced in E2F1-null (E2F1-/-) mice and WT littermates. E2F1-/- displayed an accelerated wound healing including wound closure, dermal thickening and collagen deposition, which was associated with an increased endothelial cell proliferation and greater vessel density in the border zone of the wound. Furthermore, more macrophages were recruited to the skin lesions and the level of VEGF expression was markedly higher in E2F1-/- than in WT mice.
conclusionsE2F1 hinders skin wound healing by suppressing VEGF expression, neovascularization, and macrophage recruitment. Strategies that target E2F1 may enhance wound healing.
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Registered trials
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