ArticleScientific reports2020
Skin wound closure delay in metabolic syndrome correlates with SCF deficiency in keratinocytes.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Puerarin Reverses UV-Induced Epigenetic Silencing of the Wnt/β-Catenin-KIT Axis to Mitigate Skin Fibroblast Aging.International journal of molecular sciences · 2026Article
- The Promotion of Cell Proliferation by Food-Derived Bioactive Peptides: Sources and Mechanisms.Metabolites · 2025Review
- Metabolic syndrome and its effect on immune cells in apical periodontitis- a narrative review.Clinical oral investigations · 2025Review
- Preparing the soil: Adjusting the metabolic health of patients with chronic wounds and musculoskeletal diseases.International wound journal · 2024Review
- Peripheral artery disease mediating the effect of metabolic syndrome related diseases on lower limb ulcers: Mendelian randomization analysis.Frontiers in endocrinology · 2024Article
- An Overview of Growth Factors as the Potential Link between Psoriasis and Metabolic Syndrome.Journal of clinical medicine · 2023Review
- A Novel Peptide fromToxins · 2022Article
- Highly conserved shifts in ubiquitin-proteasome system (UPS) activity drive mitochondrial remodeling during quiescence.Nature communications · 2022Article
- Histology Scoring System for Murine Cutaneous Wounds.Stem cells and development · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Poor wound closure due to diabetes, aging, stress, obesity, alcoholism, and chronic disease affects millions of people worldwide. Reasons wounds will not close are still unclear, and current therapies are limited. Although stem cell factor (SCF), a cytokine, is known to be important for wound repair, the cellular and molecular mechanisms of SCF in wound closure remain poorly understood. Here, we found that SCF expression in the epidermis is decreased in mouse models of delayed wound closure intended to mimic old age, obesity, and alcoholism. By using SCF conditionally knocked out mice, we demonstrated that keratinocytes' autocrine production of SCF activates a transient c-kit receptor in keratinocytes. Transient activation of the c-kit receptor induces the expression of growth factors and chemokines to promote wound re-epithelialization by increasing migration of skin cells (keratinocytes and fibroblasts) and immune cells (neutrophils) to the wound bed 24-48 h post-wounding. Our results demonstrate that keratinocyte-produced SCF is essential to wound closure due to the increased recruitment of a unique combination of skin cells and immune cells in the early phase after wounding. This discovery is imperative for developing clinical strategies that might improve the body's natural repair mechanisms for treating patients with wound-closure pathologies.
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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.