ArticleScientific reports2023
A new fasciocutaneous flap model identifies a critical role for endothelial Notch signaling in wound healing and flap survival.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Inorganic materials to prevent liquefactive necrosis and improve wound healing: A role of infection control across ischemic models.Materials today. Bio · 2026Article
- Comparative Analysis of Animal Models in Wound Healing Research and the Utility for Humanized Mice Models.Advances in wound care · 2025Review
- Bletilla striata polysaccharide induces autophagy through PI3K/AKT signaling pathway to promote the survival of cross-boundary flap in rats.Frontiers in pharmacology · 2025Article
- A refined experimental model for local, interpolated flap, and free tissue transfer studies using musculus cutaneus maximus-based musculocutaneous flap in the rat.Acta cirurgica brasileira · 2025Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Flap surgery is a common treatment for severe wounds and a major determinant of surgical outcome. Flap survival and healing depends on adaptation of the local flap vasculature. Using a novel and defined model of fasciocutaneous flap surgery, we demonstrate that the Notch ligand Delta-like 1 (Dll1), expressed in vascular endothelial cells, regulates flap arteriogenesis, inflammation and flap survival. Utilizing the stereotyped anatomy of dorsal skin arteries, ligation of the major vascular pedicle induced strong collateral vessel development by end-to-end anastomosis in wildtype mice, which supported flap perfusion recovery over time. In mice with heterozygous deletion of Dll1, collateral vessel formation was strongly impaired, resulting in aberrant vascularization and subsequent necrosis of the tissue. Furthermore, Dll1 deficient mice showed severe inflammation in the flap dominated by monocytes and macrophages. This process is controlled by endothelial Dll1 in vivo, since the results were recapitulated in mice with endothelial-specific deletion of Dll1. Thus, our model provides a platform to study vascular adaptation to flap surgery and molecular and cellular regulators influencing flap healing and survival.
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