Abstract
Pneumoconiosis is the most common and severe occupational disease, has become a major public health problem in the world. Its causes are well known, but the pathogenesis of it is not completely clear and effective therapies are not currently available. Epigenetic modifications have been considered an initial event in the development of pneumoconiosis. Epigenetic regulatory mechanisms in pneumoconiosis include DNA methylation, non-coding RNA (ncRNA) , and histone modification. In recent years, many researchers have studied the effect of dust-induced pulmonary fibrosis-related gene expression at the epigenetic level on macrophage activation, lung fibroblast proliferation, activation, transdifferentiation, and epithelial or endothelial-mesenchymal transition (EMT/EndMT) to further elucidate the pathogenesis of pneumoconiosis. In this review, we discusses the epigenetic modifications in pneumoconiosis, with an aim to provide new insights into the early diagnosis, condition assessment and targeted therapy of this occupational disease.
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