The organ chip model is currently regarded as one of the most promising in vitro models. By incorporating physical and chemical parameters and integrating iPS technology, disease models that better reflect pathological and physiological conditions can be developed, overcoming limitations of traditional experiments that lack cell and tissue interactions, as well as species differences. In 2010, Inberg proposed the concept of lung chips (insert literature), which has since been used successfully to simulate lung-related diseases (insert literature). Recently, Qin Jianhua and team (insert literature) constructed an in vitro lung injury model for COVID-19 using a lung organ chip. This model reproduced the process of vascular barrier damage and immune cell recruitment after virus infection, verified the antiviral effect of remdesivir, and demonstrated the reduction of pulmonary vascular barrier damage caused by the virus. This study provides a new platform for COVID-19 drug screening. Considering its enormous potential, our research team has independently developed a high-throughput lung organ chip and successfully constructed a smoke inhalation lung injury model based on this chip. Using this model, we were able to replicate alveolar vascular barrier damage caused by smoke exposure in vitro and observe phenomena such as oxidative stress, apoptosis, and inflammatory cell infiltration while exploring potential mechanisms through biochemical and protein mass spectrometry techniques. Our findings revealed iron death in smoke inhalation lung injury for the first time through chip analysis. Moreover, we verified that glucocorticoids administered via the airway or intravenous vitamin C can alleviate oxidative stress damage caused by SI-ALI. To our knowledge, this is the first report employing organoid chip technology to model smoke inhalation lung injury, providing new insights into disease mechanism research and drug development.
