Multiscale bioprinted arterial models recapitulate synergistic microenvironmental interactions in vascular disease

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Arterial microenvironment disturbances, including hemodynamic abnormalities, risk factors, and disrupted cell-cell interactions, drive cardiovascular and metabolic diseases, yet current models lack the structural and functional complexity to study these perturbations. We present extrusion-on-demand (EoD) bioprinting to engineer arterial models with microscale fidelity (triple-layered intima, media, and adventitia) and customizable macroscale geometries. These models demonstrated enhanced endothelial function and barrier integrity through layer-specific gene/protein expression, mirroring native arterial physiology. Under atherogenic factors, the platform recapitulated key atherosclerotic events—endothelial activation, monocyte infiltration, and foam cell formation—while oscillatory flow activated mechanosensitive pathways driving inflammation. Structural deficits amplified inflammatory responses, whereas nuclear factor κB (NF-κB) inhibition restored endothelial homeostasis under biochemical and hemodynamic stress. By unifying multiscale structural fidelity with dynamic microenvironmental regulation, EoD bridges the gap between simplistic in vitro systems and in vivo complexity. This approach establishes a physio-mimetic platform to dissect disease mechanisms, evaluates microenvironment-specific therapies, and advances personalized interventions for cardiovascular pathologies.

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