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Abstract
Occupational lung disease (OLD) is a group of lung diseases caused and/or aggravated by organic and inorganic inhaled dust, fumes, and mist. OLD can develop under various occupational situations. Therefore, occupational history should be considered when evaluating respiratory symptoms. Once OLD is developed, it may not be treated and may even progress after exposure to the causative agents has stopped. The best ways to treat OLD are prevention and early detection by controlling the working environment and conducting regular surveillance of workers. Common OLDs in Korea are coal worker's pneumoconiosis, asbestos-related diseases, and occupational asthma. Recent aspects of these common OLDs in Korea will be described based on recently published studies.
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Figure 2
Asbestos has pleiotropic effects on cell signaling pathways. Either through direct interactions with receptors or via the generation of reactive oxygen species (ROS), asbestos activates cell signaling pathways that regulate gene expression and cell fate. Direct interaction with the epidermal growth factor receptor (EGFR) activates the Ras-Raf-extracellular signal-regulated kinase (ERK) pathway, which controls expression and transcriptional activity of the Fos family members of the activator protein-1 (AP-1) transcription factor. Asbestos also regulates c-Jun by activating ERK5. AP-1, ERK1/2, and ERK5 govern outcomes, including cell proliferation, cell migration, and aspects of neoplastic transformation. Activation of the phosphoinositol-3 kinase (PI3K)/AKT pathway promotes cell survival through nuclear factor (NF)-kB. Recent work also indicates that asbestos fibers and ROS activate signaling through the tumor necrosis factor (TNF) receptor. The diverse phenotypic outcomes of asbestos exposure depend on fiber type, fiber dose, and the signaling pathways in specific cell types. Moreover, the physical properties of asbestos tend to promote robust and persistent activation of ERK signaling and other redox-responsive kinase cascades.
References
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