ArticleThe American journal of pathology2010
Lack of CXC chemokine receptor 3 signaling leads to hypertrophic and hypercellular scarring.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mesenchymal stem cell therapy in hypertrophic and keloid scars.Cell and tissue research · 2021Pooled it
- A catalytically active and recyclable bioelastomer inspired by metalloenzymes.Bioactive materials · 2026Article
- Cellular and Molecular Mechanisms of Wound Repair: From Biology to Therapeutic Innovation.Cells · 2025Review
- CXCR3-activating peptide inhibits pulmonary fibrosis in a bleomycin mouse model.Respiratory research · 2025Article
- An Updated Review of Hypertrophic Scarring.Cells · 2023Review
- Evolution, Expression and Functional Analysis of CXCR3 in Neuronal and Cardiovascular Diseases: A Narrative Review.Frontiers in cell and developmental biology · 2022Review
- Gene expression profile analysis on different stages of hypertrophic scarring in a rabbit ear model.Experimental and therapeutic medicine · 2020Article
- Prediction of severity and subtype of fibrosing disease using model informed by inflammation and extracellular matrix gene index.PloS one · 2020Article
- Potential therapeutic manipulations of the CXCR3 chemokine axis for the treatment of inflammatory fibrosing diseases.F1000Research · 2020Article
- Inflammation as an orchestrator of cutaneous scar formation: a review of the literature.Plastic and aesthetic research · 2020Article
- T-cell positioning by chemokines in autoimmune skin diseases.Immunological reviews · 2019Review
- Wound Healing: A Cellular Perspective.Physiological reviews · 2019Review
- A systems perspective of heterocellular signaling.Essays in biochemistry · 2018Review
- Pigment Epithelium-Derived Factor (PEDF) as a Regulator of Wound Angiogenesis.Scientific reports · 2018Article
- Clusterization of patients with idiopathic pulmonary fibrosis with chemokine receptors: a possible role in the diagnostic work-up of idiopathic pulmonary fibrosis?Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2018Article
- Article
- Multipotent stromal cells/mesenchymal stem cells and fibroblasts combine to minimize skin hypertrophic scarring.Stem cell research & therapy · 2017Article
- Loss of epidermal AP1 transcription factor function reduces filaggrin level, alters chemokine expression and produces an ichthyosis-related phenotype.Cell death & disease · 2017Article
- Improved Transplanted Stem Cell Survival in a Polymer Gel Supplemented With Tenascin C Accelerates Healing and Reduces Scarring of Murine Skin Wounds.Cell transplantation · 2017Article
- Chemokine Signaling during Midline Epithelial Seam Disintegration Facilitates Palatal Fusion.Frontiers in cell and developmental biology · 2017Article
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6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CXC chemokine receptor 3 (CXCR3) signaling promotes keratinocyte migration while terminating fibroblast and endothelial cell immigration into wounds; this signaling also directs epidermal and matrix maturation. Herein, we investigated the long-term effects of failure to activate the "stop-healing" CXCR3 axis. Full-thickness excisional wounds were created on CXCR3 knockout((-/-)) or wild-type mice and examined at up to 180 days after wounding. Grossly, the CXCR3(-/-) mice presented a thick keratinized scar compared with the wild-type mice in which the scar was scarcely noticeable; histological examination revealed thickening of both the epidermis and dermis. The dermis was disorganized with thick and long collagen fibrils and contained excessive collagen content in comparison with the wild-type mice. Interestingly, the CXCR3(-/-) wounds presented lower tensile/burst strength, which correlates with decreased alignment of collagen fibers, similar to published findings of human scars. Persistent Extracellular matrix turnover and immaturity was shown by the elevated expression of proteins of the immature matrix as well as expression of matrix metallopeptidase-9 MMP-9. Interestingly, the scars in the CXCR3(-/-) mice presented evidence of de novo development of a sterile inflammatory response only months after wounding; earlier periods showed resolution of the initial inflammatory stage. These in vivo studies establish that the absence of CXCR3(-/-) signaling network results in hypertrophic and hypercellular scarring characterized by on-going wound regeneration, cellular proliferation, and scars in which immature matrix components are undergoing increased turnover resulting in a chronic inflammatory process.
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