Pneumoconiosis is an occupational lung disease that is mainly caused by diffuse fibrosis of lung tissue due to long-term inhalation of productive dust during occupational activities and retention in the lungs. Macrophages, epithelial cells and other cells can release a large number of cytokines, such as transforming growth factor-β, monocyte chemotactic protein-1, etc. These cytokines can participate in pathologies such as local injury, inflammatory response, and pulmonary fibrosis. This article reviews the role of cytokines in the pathogenesis of pneumoconiosis in order to provide a basis for further research.

Pneumoconiosis is an occupational lung disease that is mainly caused by diffuse fibrosis of lung tissue due to long-term inhalation of productive dust during occupational activities and retention in the lungs. Macrophages, epithelial cells and other cells can release a large number of cytokines, such as transforming growth factor-β, monocyte chemotactic protein-1, etc. These cytokines can participate in pathologies such as local injury, inflammatory response, and pulmonary fibrosis. This article reviews the role of cytokines in the pathogenesis of pneumoconiosis in order to provide a basis for further research.

Idiopathic pulmonary fibrosis (IPF) is a common chronic interstitial fibrotic disease. During the fibrosis process, myofibroblasts are abnormally activated, collagen is deposited in large quantities and the biomechanical characteristics of lung tissue are significantly altered. In this paper, a systematic review about the changes in lung tissues, cellular biomechanical properties and biomechanical signals during the process of IPF was presented, and the in vitro reproduction of biomechanical features and therapeutic strategies for targeting biomechanics wassummarized, so as to provide references for clinical prevention and treatment of IPF.