Publications by authors named "Qiyue Jiang"

Silicosis is an occupational disease caused by long-term inhalation of free silica, resulting in a significant global health burden. Its pathogenesis remains unclear, and there is no effective treatment. Proliferative and activated myofibroblasts play a key role in the development of silicosis.

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Bacillus cereus is a ubiquitous foodborne pathogen commonly found in various foods. Its ability to form spores, biofilms and diarrhoeal and/or emetic toxins further exacerbates the risk of food poisoning. Violacein is a tryptophan derivative with excellent antibacterial activity.

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Silicosis is an occupational respiratory disease caused by long-term inhalation of high concentrations of free silica particles. Studies suggest that oxidative stress is a crucial initiator of silicosis fibrosis, and previous studies have linked the antioxidative stress transcription factor known as Nrf2 to fibrosis antagonism. Myofibroblasts play a pivotal role in tissue damage repair due to oxidative stress.

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Article Synopsis
  • * Previous research linked lung microbiota imbalances (dysbiosis) and metabolic changes to the development of pulmonary fibrosis, suggesting a complex relationship between microbiota and disease progression.
  • * This study used advanced sequencing and metabolomic analysis to show that silica exposure disrupts lung microbiota and metabolism, particularly affecting amino acids, which may worsen fibrosis, highlighting potential new avenues for treatment.
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Silicosis is a progressive pulmonary fibrosis disease caused by long-term inhalation of silica. The early diagnosis and timely implementation of intervention measures are crucial in preventing silicosis deterioration further. However, the lack of screening and diagnostic measures for early-stage silicosis remains a significant challenge.

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The widespread manufacture of silica and its extensive use, and potential release of silica into the environment pose a serious human health hazard. Silicosis, a severe global public health issue, is caused by exposure to silica, leading to persistent inflammation and fibrosis of the lungs. The underlying pathogenic mechanisms of silicosis remain elusive.

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Macrophage pyroptosis has recently been involved in some inflammatory and fibrosis diseases, however, the role of macrophage pyroptosis in silica-induced pulmonary fibrosis has not been fully elucidated. In this study, we explored the role of macrophage pyroptosis in silicosis in vivo and in vitro. A mouse model of silicosis was established and mice were sacrificed at 7, 14, and 28 days after exposure of silica.

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Silicosis is a fatal occupational respiratory disease caused by the prolonged inhalation of respirable silica. The core event of silicosis is the heightened activity of fibroblasts, which excessively synthesize extracellular matrix (ECM) proteins. Our previous studies have highlighted that human umbilical cord mesenchymal stem cell-derived extracellular vesicles (hucMSC-EVs) hold promise in mitigating silicosis and the significant role played by microRNAs (miRNAs) in this process.

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Silicosis is one of several potentially fatal occupational pathologies caused by the prolonged inhalation of respirable crystalline silica. Previous studies have shown that lung epithelial-mesenchymal transition (EMT) plays a significant role in the fibrosis effect of silicosis. Human umbilical cord mesenchymal stem cells-derived Extracellular vesicles (hucMSC-EVs) have attracted great interest as a potential therapy of EMT and fibrosis-related diseases.

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Silicosis is a progressive inflammatory disease with poorly defined mechanisms and limited therapeutic options. Recent studies found that microRNAs (miRNAs) and circular RNAs (circRNAs) were involved in the development of respiratory diseases; however, the function of non-coding RNAs in silicosis was still needed to be further explored. We found that miR-223-3p was significantly decreased in macrophages and lung tissues of mice after silica treatment, which were consistent with the results of GEO database microarray analysis.

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Airborne fine particulate matter (PM) is considered to be a risk factor for lung fibrosis, and therefore, it has attracted public attention due to its various physicochemical features and its adverse effects on health. However, little remains to be known regarding the mechanism of PM-induced pulmonary fibrosis. The lung microbiota may be a potential factor involved in the adverse outcomes of pulmonary fibrosis.

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Silicosis of pulmonary fibrosis (PF) is related to long-term excessive inhalation of silica. The activation of fibroblasts into myofibroblasts is the main terminal effect leading to lung fibrosis, which is of great significance to the study of the occurrence and development of silicosis fibrosis and its prevention and treatment. Exosomes derived from human umbilical cord mesenchymal stem cells (hucMSC-Exos) are considered to be a potential therapy of silica-induced PF, however, their exact mechanism remains unknown.

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The impact of PM on epithelial cells is a pivotal process leading to many lung pathological changes and pulmonary diseases. In addition to PM direct interaction with epithelia, macrophages that engulf PM may also influence the function of epithelial cells. However, among the toxic researches of PM, there is a lack of evaluation of direct or indirect exposure model on human bronchial epithelial cell against PM.

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