Affiliation:
1. Weifang Medical University Weifang Shandong China
2. Department of Public Health Jining Medical University Jining Shandong China
3. Binzhou Medical University Yantai Shandong China
Abstract
AbstractSeveral 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.
Funder
Natural Science Foundation of Shandong Province