Silica dust exposure induces pulmonary fibrosis through autophagy signaling

• DOI: 10.1002/tox.23124
• Publication Date: 2021-03-15T10:33:31Z
• Authors: Ning Li; Fan Shi; Xiaoyan Wang; Pan Yang; Kun Sun; Lin Zhang; Xiaohui Hao; Xiaoming Li; Jinlong Li; Yulan Jin
• Keywords: Silicosis

Abstract Silicosis is a well‐acknowledged occupational lung disease caused by inhalation of large amount free silica dust during the production period and eventually considerable negative impact on patients' quality life. Autophagy exerts critical influence immune inflammatory responses pathogenesis pulmonary fibrosis. In this study, we sought to determine whether autophagy involved in silicosis's how it may affect cellular physiology. animal experiments, found persistent activation development fibrosis, which was also accompanied tumor necrosis factor transforming growth expression increased. Therefore, signaling pathway regulate response progression Further, vitro used LY294002, RAPA, N‐acetylcysteine (NAC) intervened autophagy. Our results showed that PI3K/Akt/mTOR changed mediated SiO 2 exposed, might play protective role Additionally, NAC's effect not apparent ‐mediated through pathway, but can reduce NR8383 cells SiO2‐exposed. Nevertheless, it's interesting NAC ‐exposed. Taken together, our data demonstrated ‐exposed induce fibrosis along with both vivo vitro, could alleviate non specific mechanism its action needs further studying.