ArticleThe Journal of experimental medicine2015
The Dishevelled-binding protein CXXC5 negatively regulates cutaneous wound healing.
Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 59 citations in OpenAlex.
- Wnt11 mediates fibroblast-smooth muscle cell interaction to promote neurogenic bladder fibrosis in rats.Communications biology · 2026Article
- Novel small molecules downregulate CDK1 expression and inhibit Wnt/β-catenin signaling in cutaneous squamous cell carcinoma by targeting its distinct tumor-specific cellular landscape.Experimental & molecular medicine · 2025Article
- CXXC5 is a ubiquitinated protein and is degraded by the ubiquitin-proteasome pathway.Protein science : a publication of the Protein Society · 2025Article
- Review
- CXXC5 function blockade promotes diabetic wound healing through stimulating fibroblast and vascular endothelial cell activation.Cell communication and signaling : CCS · 2025Article
- HEALS-A and GRADES: Novel Histological and Clinical Scales for Assessing Skin Regeneration in Murine Wound Healing Models.Diagnostics (Basel, Switzerland) · 2025Article
- Signal integrator function of CXXC5 in Cancer.Cell communication and signaling : CCS · 2025Review
- MiR-28-3p regulates high glucose-induced endothelial dysfunction by targeting CXXC5.Archives of medical science : AMS · 2025Article
- Inhibiting the cytosolic function of CXXC5 accelerates diabetic wound healing by enhancing angiogenesis and skin repair.Experimental & molecular medicine · 2023Article
- Mechanisms underlying pathological scarring by fibroblasts during wound healing.International wound journal · 2023Article
- KY19382 Accelerates Cutaneous Wound Healing via Activation of the Wnt/β-Catenin Signaling Pathway.International journal of molecular sciences · 2023Article
- Transcriptomic characterization of Lonrf1 at the single-cell level under pathophysiological conditions.Journal of biochemistry · 2023Article
- Article
- Blockade of CXXC5-dishevelled interaction inhibits adipogenic differentiation, obesity, and insulin resistance in mice.Scientific reports · 2022Article
- Article
- Idax and Rinf facilitate expression of Tet enzymes to promote neural and suppress trophectodermal programs during differentiation of embryonic stem cells.Stem cell research · 2022Article
- Aging Impairs the Cellular Interplay between Myeloid Cells and Mesenchymal Cells during Skin Healing in Mice.Aging and disease · 2022Article
- The interplay of fibroblasts, the extracellular matrix, and inflammation in scar formation.The Journal of biological chemistry · 2022Review
- Approaches for Regenerative Healing of Cutaneous Wound with an Emphasis on Strategies Activating the Wnt/β-Catenin Pathway.Advances in wound care · 2022Article
- The epigenetic regulator RINF (CXXC5) maintainsHaematologica · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wnt/β-catenin signaling plays important roles in cutaneous wound healing and dermal fibrosis. However, its regulatory mechanism has not been fully elucidated, and a commercially available wound-healing agent targeting this pathway is desirable but currently unavailable. We found that CXXC-type zinc finger protein 5 (CXXC5) serves as a negative feedback regulator of the Wnt/β-catenin pathway by interacting with the Dishevelled (Dvl) protein. In humans, CXXC5 protein levels were reduced in epidermal keratinocytes and dermal fibroblasts of acute wounds. A differential regulation of β-catenin, α-smooth muscle actin (α-SMA), and collagen I by overexpression and silencing of CXXC5 in vitro indicated a critical role for this factor in myofibroblast differentiation and collagen production. In addition, CXXC5(-/-) mice exhibited accelerated cutaneous wound healing, as well as enhanced keratin 14 and collagen synthesis. Protein transduction domain (PTD)-Dvl-binding motif (DBM), a competitor peptide blocking CXXC5-Dvl interactions, disrupted this negative feedback loop and activated β-catenin and collagen production in vitro. Co-treatment of skin wounds with PTD-DBM and valproic acid (VPA), a glycogen synthase kinase 3β (GSK3β) inhibitor which activates the Wnt/β-catenin pathway, synergistically accelerated cutaneous wound healing in mice. Together, these data suggest that CXXC5 would represent a potential target for future therapies aimed at improving wound healing.
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