The role of mitochondrial dysfunction in macrophages on SiO2‐induced pulmonary fibrosis: A review

• Published in: Journal of applied toxicology Vol. 44; no. 1; pp. 86 - 95
• Main Authors: Zhao, Jia‐hui, Li, Shuang, Du, Shu‐ling, Zhang, Zhao‐qiang
• Format: Journal Article
• Language: English
• Published: Bognor Regis Wiley Subscription Services, Inc 01.01.2024
• Subjects: Abnormalities; Alveoli; Dust; Epidemiology; Fibrosis; Lung diseases; macrophage mitochondrial dysfunction; Macrophages; Mitochondria; Molecular modelling; Pathogenesis; pulmonary fibrosis; ROS: ATP; Silica; Silicon dioxide; Silicosis; Toxicity testing
• ISSN: 0260-437X; 1099-1263
• DOI: 10.1002/jat.4517

Several epidemiologic and toxicological studies have widely regarded that mitochondrial dysfunction is a popular molecular event in the process of silicosis from different perspectives, but the details have not been systematically summarized yet. Thus, it is necessary to investigate how silica dust leads to pulmonary fibrosis by damaging the mitochondria of macrophages. In this review, we first introduce the molecular mechanisms that silica dust induce mitochondrial morphological and functional abnormalities and then introduce the main molecular mechanisms that silica‐damaged mitochondria induce pulmonary fibrosis. Finally, we conclude that the mitochondrial abnormalities of alveolar macrophages caused by silica dust are involved deeply in the pathogenesis of silicosis through these two sequential mechanisms. Therefore, reducing the silica‐damaged mitochondria will prevent the potential occurrence and fatality of the disease in the future. Mitochondrial dysfunction is a popular molecular event in the formation of silicosis, but the details have not been systematically summarized yet. In this review, we first introduce the molecular mechanisms that silica dust induce mitochondrial abnormalities and then introduce the main molecular mechanisms that silica‐damaged mitochondria induce pulmonary fibrosis. Finally, we conclude that the mitochondrial abnormalities of alveolar macrophages caused by silica dust are involved deeply in the pathogenesis of silicosis through these two sequential mechanisms.