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Atherosclerosis is a complex, multifactorial disease driven by intricate cellular and molecular interactions within the vascular microenvironment. While conventional experimental models have provided important insights into disease progression, they often fail to recapitulate the coupled mechanical and biochemical stimuli that govern vascular pathology in vivo. Lab-on-a-chip technologies offer a powerful platform for reconstructing key cellular and tissue-level features of atherosclerosis within controlled microscale environments, enabling the study of processes such as endothelial dysfunction, inflammatory signaling, cell-matrix interactions, and vascular remodeling. The integration of microfluidics further enhances these models by enabling precise control of flow-derived mechanical cues, including shear stress, vascular geometry, and pulsatile pressure. This review highlights recent advances in microfluidic lab-on-a-chip models for atherosclerosis research, with a focus on their ability to replicate human-relevant pathophysiological conditions. We discuss pioneering studies that have employed these paltforms to investigate endothelial barrier dysfunction, monocyte recruitment, foam cell formation, vascular remodeling, and plaque instability across different stages of disease progression. Collectively, these microfluidic systems provide powerful, physiologically relevant tools for dissecting the mechanisms underlying atherosclerosis and evaluating therapeutic strategies under controlled, biomimetic vascular conditions.
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Akther et al. (2026) studied this question.
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