Lymphangiogenesis is Critical for Healing and Survival in a Murine Model of Laryngotracheal Injury

In C57BL6 mice with laryngotracheal stenosis, blocking VEGFR-3–dependent lymphangiogenesis with SAR131675 abrogates lymphatic vessel expansion and markedly increases mortality.

• Why it matters: Lymphatic dysfunction is linked to worse fibrosis in other diseases, but its role in airway mucosal injury and healing after laryngotracheal injury was unknown.
• What they did: Using a chemomechanical LTS injury model, the study quantified subepithelial lymphatics by LYVE-1 immunohistochemistry and treated mice with the VEGFR-3 inhibitor SAR131675 to block lymphangiogenesis.
• The result: SAR131675-treated mice showed impaired epithelial repair with obstructive sloughing, increased edema, persistent tissue injury on histopathology, and qualitative fibrocellular remodeling changes without lamina propria thickness differences.

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