Low-level PM_2.5 induces the occurrence of early pulmonary injury by regulating circ_0092363

The significant correlation between particulate matter with aerodynamic diameters of ≤ 2.5 µm (PM_2.5) and the high morbidity and mortality of respiratory diseases has become the consensus of the research. Epidemiological studies have clearly pointed out that there is no safe concentration of PM_2.5, and mechanism studies have also shown that exposure to PM_2.5 will first cause pulmonary inflammation. Therefore, the purpose of this study is to explore the mechanism of early lung injury induced by low-level PM_2.5 from the perspective of epigenetics. Based on the previous results of population samples, combined with an in vitro/vivo exposure model of PM_2.5, it was found that low-level PM_2.5 promoted the transport of circ_0092363 from intracellular to extracellular spaces. The decreased expression of intracellular circ_0092363 resulted in reduced absorption of miR-31-5p, leading to inhibition of Rho associated coiled-coil containing protein kinase 1 (ROCK1) and the subsequent abnormal expression of tight junction proteins such as Zonula occludens protein 1 (ZO-1) and Claudin-1, ultimately inducing the occurrence of early pulmonary injury. Furthermore, this study innovatively introduced organoid technology and conducted a preliminary exploration for a study of the relationship among environmental exposure genomics, epigenetics and disease genomics in organoids. The role of circ_0092363 in early pulmonary injury induced by low-level PM_2.5 was elucidated, and its value as a potential diagnostic biomarker was confirmed.