加热烟草产品（HTP）有望降低与吸烟相关的心血管疾病（CVD）的风险。然而，对HTP对动脉粥样硬化的影响进行机制研究仍然不足，需要开展更多人类相关情况下的研究，以更深入地了解HTP降低风险潜力。在本研究中，我们首先通过考虑巨噬细胞产生的促炎症细胞因子介导的内皮细胞活化，利用芯片上的器官（OoC）开发了一种单核细胞黏附的体外模型，为模拟人体生理的主要方面提供了巨大机会。然后，根据单核细胞黏附方面比较了三种不同类型的HTP产生的气溶胶与香烟烟雾（CS）的生物活性。我们的模型显示，肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）的有效浓度范围接近CVD发病的实际情况。该模型还显示，单核细胞黏附由于分泌较少的促炎症因子而不会被每种HTP气溶胶诱导，这可能是由于较少的促炎症因子分泌所致。总之，我们的血管芯片模型评估了香烟和HTP生物效应的差异，并提示HTP对动脉粥样硬化降低风险的潜力。 版权所有©2023。由Elsevier Ltd.出版。

Heated tobacco products (HTPs) are expected to have the potential to reduce risks of smoking-associated cardiovascular disease (CVD). However, mechanism-based investigations of the effect of HTPs on atherosclerosis remain insufficient and further studies under human-relevant situations are desired for deeper understanding of the reduced risk potential of HTPs. In this study, we first developed an in vitro model of monocyte adhesion by considering macrophage-derived proinflammatory cytokine-mediated endothelial activation using an organ-on-a-chip (OoC), which provided great opportunities to mimic major aspects of human physiology. Then biological activities of aerosol from three different types of HTPs in terms of monocyte adhesion were compared with that of cigarette smoke (CS). Our model showed that the effective concentration ranges of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were close to the actual condition in CVD pathogenesis. The model also showed that monocyte adhesion was less induced by each HTP aerosol than CS, which may be caused by less proinflammatory cytokine secretion. In summary, our vasculature-on-a-chip model assessed the difference in biological effects between cigarettes and HTPs, and suggested a reduced risk potential of HTPs for atherosclerosis.Copyright © 2023. Published by Elsevier Ltd.