A Novel Mouse Model for Venous High-Load Remodeling Induced by Unilateral Jugular Vein Transection

Abstract

Chronic venous disease (CVD) is a prevalent peripheral vascular disorder characterized by vascular remodeling driven by hemodynamic overload, yet available animal models are limited by high surgical difficulty and unstable induction efficiency. Here, we developed a novel mouse venous high-load remodeling model by selectively ablating the unilateral cervical venous drainage system. After 4 weeks, compensatory contralateral jugular veins were assessed via ultrasonography, histology, Western blot, and bulk RNA sequencing. The model displayed marked luminal dilation, wall hypertrophy, and excessive collagen deposition, along with downregulated smooth muscle contractile markers (α-SMA, SM22α) and upregulated adhesion molecule ICAM-1. Transcriptomic profiling identified 252 differentially expressed genes, predominantly enriched in extracellular matrix organization, angiogenesis, and complement-coagulation cascades, suggesting potential pathways involved in the venous remodeling process. This model reliably recapitulates the pathological features associated with hemodynamic overload-induced venous remodeling, offering a valuable tool for investigating CVD pathogenesis and intervention targets.