ArticleThe Journal of investigative dermatology2010
Persistent inflammation and angiogenesis during wound healing in K14-directed Hoxb13 transgenic mice.
Article in The Journal of investigative dermatology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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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
10 citing papers in PubMed, 25 citations in OpenAlex.
- Diminished γδ T Cells during Murine Allergic Skin Inflammation Is Mediated by IL-4 Signaling in Keratinocytes.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- HOXB13 expression is correlated with hepatic inflammatory activity of patients with hepatic fibrosis.Journal of molecular histology · 2020Article
- Homeobox B9 facilitates hypertrophic scar formation via activating the mitogen-activated protein kinase signaling pathway.Molecular medicine reports · 2017Article
- Insulin treatment prevents wounding associated changes in tissue and circulating neutrophil MMP-9 and NGAL in diabetic rats.PloS one · 2017Article
- Transition from inflammation to proliferation: a critical step during wound healing.Cellular and molecular life sciences : CMLS · 2016Review
- Roles of Proteoglycans and Glycosaminoglycans in Wound Healing and Fibrosis.International journal of cell biology · 2015Review
- High-level expression of HOXB13 is closely associated with tumor angiogenesis and poor prognosis of hepatocellular carcinoma.International journal of clinical and experimental pathology · 2014Article
- Angiogenesis-related biomarkers in patients with alcoholic liver disease: their association with liver disease complications and outcome.Mediators of inflammation · 2014Article
- Prevalence of immune disease in patients with wounds presenting to a tertiary wound healing centre.International wound journal · 2012Article
- The dual roles of homeobox genes in vascularization and wound healing.Cell adhesion & migrationReview
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Chronic, nonhealing wounds and inadequate tissue repair characterized by excessive fibrosis continue to have a considerable negative effect on health and quality of life. Understanding the molecular events required for adequate healing, including the transcriptional control of wound repair, will be important for the development of future therapies. We previously showed that loss of Hoxb13 from murine skin results in enhanced cutaneous wound healing, suggesting that Hoxb13 has a negative effect on wound repair. To test this, we generated skin-specific Hoxb13 transgenic (TG) mice that overexpress Hoxb13 in the basal layer of the epidermis by the human keratin 14 promoter. Using these mice, we evaluated the effects of Hoxb13 overexpression on cutaneous wound healing. Transgenic wounds were characterized by persistence of the fibrin clot and prolonged inflammation. Notably, neutrophils, which had cleared from wild-type wounds, were still pronounced in TG wounds. Marked epidermal hyperplasia was observed at TG wound edges, and dermal vessels were grossly abnormal compared with wild-type mice. Both vascular endothelial growth factor and tumor necrosis factor-alpha were upregulated in Hoxb13 TG skin. Together, our results identify Hoxb13 as a potential important clinical target in wound healing and other pathologies characterized by abnormal or excessive inflammation, angiogenesis, or epidermal proliferation.
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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.