To investigate the mortality probability, life expectancy of coal workers’ pneumoconiosis (CWP), and related factors of life expectancy, a total of 495 patients with CWP were diagnosed and reported from 1963 to 2014 in a state-owned mine in the east of China. The life table method, log rank method, and Cox regression model were used for survival analysis. 95 out of 495 CWP died during this period. The mortality rate was 19.19%. The average life span was 12.1 (0.0–33.2) years and average death age was 57.4 (33.0–83.0) years. The life table indicated that overall mortality probability increased with the age of CWP patients. Life expectancy of CWP patients was prolonged to 4.3, 1.4, 1.2, and 1.4 years without death caused by pneumoconiosis, tuberculosis, lung cancer, and pulmonary heart disease respectively. The survival curve of CWP patients without pulmonary tuberculosis was higher (average 37.9 years) than patients with pulmonary tuberculosis (average 34.1 years). There was significant difference observed (χ² = 6.196, p < 0.05). Three risk factors that include initial dust exposure year, age of onset, and first diagnostic stage were put into the Cox regression model for evaluation. The data indicated that prevention and treatment of CWP complication is important to improve patients’ survival rates.

Coal Workers’ Pneumoconiosis (CWP) is the primary occupational disease in China. However, information about the definite prevalence of CWP is only partially available. The aims of our study were to assess the prevalence characteristics of CWP in a state-owned coal mine, evaluate the effects of control measures and develop further preventive strategies for CWP. The total study population included 495 cases who were diagnosed with CWP from the construction of this coal mine to the end of October 2014. Individuals’ information, including duration of dust exposure, job titles, age as first diagnosis, stages of CWP, CWP progress, complications with pulmonary tuberculosis, death and others were collected and analyzed. The results showed that 71.11% of 495 CWP cases were stage I and 90.71% were involved in tunneling or coal mining. The mean dust exposure period in CWP patients was 26.7 years, the mean latent period was 29.3 years and the mean diagnosed age was 50.3 years old. The proportion of CWP diagnosed after ending dust exposure were remarkably increased with the time passing. Among the CWP cases, 36 (7.27%) were complicated with pulmonary tuberculosis. The mortality of patients with stage III was the highest (60.71%) (p < 0.0001). Our data obviously show that more strict policies to protect coal miners are needed to be implemented in China, especially for tunneling and mining workers.

Existing studies reported that some circular RNAs (circRNAs) play vital roles in the development of pulmonary fibrosis. However, few studies explored the biomarker potential of circRNAs for pulmonary fibrosis based on population data. Therefore, we aimed to identify peripheral blood circRNAs as potential biomarkers for diagnosing silicosis and idiopathic pulmonary fibrosis (IPF). In brief, an RNA-seq screening based on 4 silicosis cases and 4 controls was initially performed. Differentially expressed circRNAs were combined with the human serum circRNA dataset to identify overlapping serum-detectable circRNAs, followed by validation using the GEO dataset (3 IPF cases and 3 controls) and subsequent qRT-PCR, including 84 additional individuals. Following the above steps, 243 differentially expressed circRNAs were identified during the screening stage, with fold changes ≥ 1.5 and P < 0.05. Of note, the human serum circRNA dataset encompassed 28 of 243 circRNAs. GEO (GSE102660) validation revealed two highly expressed circRNAs (P < 0.05) in the IPF case group. Furthermore, at the enlarged sample validation stage, hsa_circ_0058493 was highly expressed in both silicosis and IPF cases (silicosis: P = 1.16 × 10^-6; IPF: P = 7.46 × 10^-5). Additionally, hsa_circ_0058493 expression was significantly increased in MRC-5 cells upon TGF-β1 treatment, while hsa_circ_0058493 knockdown inhibited the expression of fibrotic molecules by affecting the epithelial-mesenchymal transition process. These shreds of evidence indicated that hsa_circ_0058493 might serve as a novel biomarker for diagnosing silicosis and IPF.

Silicosis is associated with fibroblast proliferation and extracellular matrix deposition in lung tissues. The dysregulation of miR-1224-5p has been implicated in several human cancers; however, the expression and function of miR-1224-5p in silicosis is unknown. The mitochondrial dysfunctions play critical roles in some diseases, but how these processes are regulated in silicosis remains limited. Here, we explored the role of miR-1224-5p in a mouse model of silicosis. We showed that the expression of miR-1224-5p is increased both in lung tissues of silica-induced pulmonary fibrosis and fibroblasts exposed to TGF-β1. Repression of miR-1224-5p expression attenuated silica-induced fibrotic progression in vivo and TGF-β1-induced myofibroblast differentiation in vitro. Additionally, we demonstrated that miR-1224-5p facilitated silica-induced pulmonary fibrosis primarily by repressing one of target genes, BECN1, thereby blocking PARK2 translocation to mitochondria and inducing the accumulation of damaged mitochondria. Furthermore, the activation of PDGFR signal mediated by mitochondrial damage and insufficient mitophagy resulted in myofibroblast differentiation. Collectively, these data indicated that miR-1224-5p exerts key functions in silica-induced pulmonary fibrosis and may represent a potential therapeutic target for silicosis.

Inhalation and deposition of crystalline silica particles in the lung can cause pulmonary fibrosis, then leading to silicosis. Given the paucity of effective drugs for silicosis, new insights for understanding the mechanisms of silicosis, including lung fibroblast activation and myofibroblast differentiation, are essential to explore therapeutic strategies. Our previous research showed that the up‐regulation of miR‐503 alleviated silica‐induced pulmonary fibrosis in mice. In this study, we investigated whether miR‐503 can regulate the TGF‐β1‐induced effects in lung fibroblasts. Mimic‐based strategies aiming at up‐regulating miR‐503 were used to discuss the function of miR‐503 in vivo and in vitro. We found that the expression level of miR‐503 was decreased in fibroblasts stimulated by TGF‐β1, and the up‐regulation of miR‐503 reduced the release of fibrotic factors and inhibited the migration and invasion abilities of fibroblasts. Combined with the up‐regulation of miR‐503 in a mouse model of silica‐induced pulmonary fibrosis, we revealed that miR‐503 mitigated the TGF‐β1‐induced effects in fibroblasts by regulating VEGFA and FGFR1 and then affecting the MAPK/ERK signalling pathway. In conclusion, miR‐503 exerted protective roles in silica‐induced pulmonary fibrosis and may represent a novel and potent candidate for therapeutic strategies in silicosis.