Silicon dioxide-induced endoplasmic reticulum stress of alveolar macrophages and its role on the formation of silicosis fibrosis: a review article.

Abstract

Silicosis is a chronic lung inflammatory disease induced by long-term inhalation of high concentrations of silicon dioxide (SiO2), characterized by pulmonary fibrosis. Inhalation of silica invades alveolar macrophages (AMs) and changes the micro-environment of the cell, resulting in abnormal morphology and dysfunction of the endoplasmic reticulum (ER). Once beyond the range of cell regulation, the endoplasmic reticulum stress (ERS) will occur, which will lead to cell damage, necrosis, and apoptosis, eventually causing silicosis fibrosis through various mechanisms. This is a complex and delicate process accompanied by various macrophage-derived cytokines. Unfortunately, the details have not been systematically summarized yet. In this review, we systematically introduce the basic two processes: the process of inducing ERS by inhaling SiO2 and the process of inducing pulmonary fibrosis by ERS. Moreover, the underlying mechanism of the above two sequential events is also be discussed. We conclude that the ERS of alveolar macrophages caused by silica dust are involved deeply in the pathogenesis of silicosis. Therefore, changing the states of SiO2-induced ERS of macrophage may be an attractive therapeutic target for silicosis fibrosis.