ArticleThe British journal of dermatology2015
Topical axitinib suppresses angiogenesis pathways induced by pulsed dye laser.
Article in The British journal of dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- A Randomized Controlled Pilot Study: Combined 595-nm Pulsed Dye Laser Treatment and Oxymetazoline Hydrochloride Topical Cream Superior to Oxymetazoline Hydrochloride Cream for Erythematotelangiectatic Rosacea.Lasers in surgery and medicine · 2021Trial
- The Diagnosis and Treatment Technology of Port-Wine Stain, and the Prospect of Future Treatment.Dermatology and therapy · 2026Review
- EndothelialFrontiers in cell and developmental biology · 2025Article
- Current clinical evidence is insufficient to support HMME-PDT as the first choice of treatment for young children with port wine birthmarks.Lasers in surgery and medicine · 2024Review
- Sturge-Weber Syndrome: A Review of Pathophysiology, Genetics, Clinical Features, and Current Management Approache.The application of clinical genetics · 2023Review
- Intralesional Axitinib Injection Mitigates Hypertrophic Scar by Inhibiting Angiogenesis Pathway: A Preliminary Study in a Rabbit Ear Model.Clinical, cosmetic and investigational dermatology · 2023Article
- Pathogenesis of Port-Wine Stains: Directions for Future Therapies.International journal of molecular sciences · 2022Review
- Whole-Genome Sequencing IdentifiedFrontiers in medicine · 2022Article
- GNAQ mutations drive port wine birthmark-associated Sturge-Weber syndrome: A review of pathobiology, therapies, and current models.Frontiers in human neuroscience · 2022Review
- Site-specific pharmaco-laser therapy: A novel treatment modality for refractory port wine stains.Journal of clinical and translational research · 2019Review
- The Pathogenesis of Port Wine Stain and Sturge Weber Syndrome: Complex Interactions between Genetic Alterations and Aberrant MAPK and PI3K Activation.International journal of molecular sciences · 2019Review
- Tumor-educated platelet miR-34c-3p and miR-18a-5p as potential liquid biopsy biomarkers for nasopharyngeal carcinoma diagnosis.Cancer management and research · 2019Article
- Coexistence of Eph receptor B1 and ephrin B2 in port-wine stain endothelial progenitor cells contributes to clinicopathological vasculature dilatation.The British journal of dermatology · 2017Article
- Ultrastructural characterization of hyperactive endothelial cells, pericytes and fibroblasts in hypertrophic and nodular port-wine stain lesions.The British journal of dermatology · 2017Article
- Activation of PKCα and PI3K Kinases in Hypertrophic and Nodular Port Wine Stain Lesions.The American Journal of dermatopathology · 2017Article
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Authors and funding
11 authors.
Funding
Abstract
backgroundThe recurrence of port-wine stain (PWS) blood vessels by pulsed dye laser (PDL)-induced angiogenesis is a critical barrier that must be overcome to achieve a better therapeutic outcome.
objectivesTo determine whether PDL-induced angiogenesis can be suppressed by topical axitinib.
methodsThe mRNA expression profiles of 86 angiogenic genes and phosphorylation levels of extracellular signal regulated kinases (ERKs), phosphorylated protein kinase B (AKT) and ribosomal protein S6 kinase (p70S6K) in rodent skin were examined with or without topical axitinib administration after PDL exposure.
resultsThe PDL-induced increased transcriptional levels of angiogenic genes peaked at days 3-7 post-PDL exposure. Topical application of 0·5% axitinib effectively suppressed the PDL-induced increase in mRNA levels of the examined angiogenic genes and activation of AKT, P70S6K and ERK from days 1 to 7 post-PDL exposure. After topical administration, axitinib penetrated into rodent skin to an approximate depth of 929·5 μm.
conclusionsTopical application of 0·5% axitinib can systematically suppress the PDL-induced early stages of angiogenesis via inhibition of the AKT/mammalian target of rapamycin/p70S6K and Src homology 2 domain containing transforming protein-1/mitogen-activated protein kinase kinase/ERK pathway cascades.
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