A Multiscale Computational Model of Endothelial‐Immune Cell Interactions Regulated by Dynamic Wall Shear Stress

scenarios. These results indicate that dynamic WSS drives EC state transitions and regulates immune cell recruitment and differentiation, providing a framework for studying vascular inflammation. Spatially heterogeneous WSS induces local NO depletion, which accelerates EC activation and death in low-shear stress regions, explaining focal endothelial dysfunction. EC injury further increases MCP-1 production, enhances monocyte recruitment, and promotes macrophage polarization toward a pro-inflammatory phenotype, demonstrating the ability of the model to capture flow-dependent vascular immune dynamics and inflammatory lesion development. This work provides mechanistic insight into the interplay between mechanical forces and vascular immune responses and may guide strategies for preventing endothelial injury and promoting anti-inflammatory therapy.