FOXO1, TGF-β Regulation and Wound Healing
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Summary
The transcription factor forkhead boxO-1 (FOXO1) has recently been found to be an important regulator of wound healing and has significant effects through regulation of transforming growth factor-beta (TGF-β) expression and protecting keratinocytes from oxidative stress.
- Type
- article
- Published
- 2014-09-01
- Cited by
- 107
- References
- 77
- Access
- Open access
- OpenAlex
- https://openalex.org/W25226535
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:19349022
Keywords
Potash, Brassica, Potassium, Agronomy, Sieve (category theory)
References
- Trichinella spiralis: nurse cell formation with emphasis on analogy to muscle cell repair
- Relationship between apoptotic markers (Bax and Bcl-2) and biochemical markers in type 2 diabetes mellitus.
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- Use of the Parabiotic Model in Studies of Cutaneous Wound Healing to Define Participation of Circulating Cells
- Gene expression demonstrates increased resilience toward harmful inflammatory stimuli in the proliferating epidermis of human skin wounds
- Effect of glycaemic control on apoptosis in diabetic wounds.
- Interaction of Microbiome and the Innate Immune Response in Chronic Wounds
- PERSPECTIVE ARTICLE: Growth factors and cytokines in wound healing
- c-Jun is essential for organization of the epidermal leading edge.
- Cellular and molecular mechanisms of stress-induced premature senescence (SIPS) of human diploid fibroblasts and melanocytes.
- Impaired wound healing in mouse models of diabetes is mediated by TNF-α dysregulation and associated with enhanced activation of forkhead box O1 (FOXO1)
- Cellular and molecular facets of keratinocyte reepithelization during wound healing.
- Role of Forkhead Transcription Factors in Diabetes-Induced Oxidative Stress
- Dermal transforming growth factor-beta responsiveness mediates wound contraction and epithelial closure.
- Matrix metalloproteinases and epidermal wound repair
- Abnormal Cell Responses and Role of TNF-α in Impaired Diabetic Wound Healing
- AKT/PKB signaling: navigating downstream.
- Oxidative stress in chronic venous leg ulcers
- Overexpression of TIMP-1 under the MMP-9 promoter interferes with wound healing in transgenic mice
- TNF-α Mediates Diabetes-Enhanced Chondrocyte Apoptosis During Fracture Healing and Stimulates Chondrocyte Apoptosis Through FOXO1
Cited by
- Integrated Interaction Network of MicroRNA Target Genes in Keloid Scarring
- Impact of Diabetes on the Protective Role of FOXO1 in Wound Healing
- Transcriptome analyses of Atlantic salmon (Salmo salar L.) erythrocytes infected with piscine orthoreovirus (PRV).
- Diabetes and Its Effect on Bone and Fracture Healing
- Insight into Reepithelialization: How Do Mesenchymal Stem Cells Perform?
- Hormone-Sensing Mammary Epithelial Progenitors: Emerging Identity and Hormonal Regulation
- Nucleolin enhances the proliferation and migration of heat‐denatured human dermal fibroblasts
- Inflammatory Biomarkers in Osteoarthritis
- Dendritic cells modulate burn wound healing by enhancing early proliferation
- Epithelial-mesenchymal transition: An emerging target in tissue fibrosis
- Extracellular superoxide dismutase deficiency impairs wound healing in advanced age by reducing neovascularization and fibroblast function
- Tenogenic induction of equine mesenchymal stem cells by means of growth factors and low-level laser technology
- Mesenchymal stem cell‐conditioned medium accelerates wound healing with fewer scars
- The molecular basis of hypertrophic scars
- The effects of topical melatonin on oxidative stress, apoptosis signals, and p53 protein expression during cutaneous wound healing
- Expression of TGF-β1 and miRNA-145 in patients with diabetic foot ulcers.
- ΔNp63α silences a microRNA program to aberrantly initiate a wound healing program that promotes TGFβ-induced metastasis
- MicroRNA-483-3p Inhibits Extracellular Matrix Production by Targeting Smad4 in Human Trabecular Meshwork Cells.
- BAMBI inhibits skin fibrosis in keloid through suppressing TGF-β1-induced hypernomic fibroblast cell proliferation and excessive accumulation of collagen I.
- Investigation on the effects of the atmospheric pressure plasma on wound healing in diabetic rats
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