Dust induces lung fibrosis through dysregulated DNA methylation

Zhang, Na; Liu, Keliang; Wang, Kai; Zhou, Ci; Wang, He-Jing; Che, Shuangshuang; Liu, Zhihong; Yang, Huifang

doi:10.1002/tox.22739

Cited by 26 publications

(16 citation statements)

References 58 publications

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“…When individuals are exposed to environmental stresses, such as smoke and dust, air pollution can cause epigenetic changes. It has been shown that silica exposure increases expression of DNA methyltransferase 1 (DNMT1) in patients with IPF, leading to the accumulation of collagen and lung fibrosis ( Zhang N et al, 2019 ).…”

Section: Risk Factorsmentioning

confidence: 99%

Idiopathic Pulmonary Fibrosis: An Update on Pathogenesis

et al. 2022

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Idiopathic pulmonary fibrosis (IPF) is a progressive, lethal fibrotic lung disease that occurs primarily in middle-aged and elderly adults. It is a major cause of morbidity and mortality. With an increase in life expectancy, the economic burden of IPF is expected to continuously rise in the near future. Although the exact pathophysiological mechanisms underlying IPF remain not known. Significant progress has been made in our understanding of the pathogenesis of this devastating disease in last decade. The current paradigm assumes that IPF results from sustained or repetitive lung epithelial injury and subsequent activation of fibroblasts and myofibroblast differentiation. Persistent myofibroblast phenotype contributes to excessive deposition of the extracellular matrix (ECM) and aberrant lung repair, leading to tissue scar formation, distortion of the alveolar structure, and irreversible loss of lung function. Treatments of patients with IPF by pirfenidone and nintedanib have shown significant reduction of lung function decline and slowing of disease progression in patients with IPF. However, these drugs do not cure the disease. In this review, we discuss recent advances on the pathogenesis of IPF and highlight the development of novel therapeutic strategies against the disease.

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Section: Risk Factorsmentioning

confidence: 99%

Idiopathic Pulmonary Fibrosis: An Update on Pathogenesis

et al. 2022

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“…At the same time, DNMT1 levels were raised, which corresponds to Thy-1 promoter hypermethylation and a decrease in Thy-1 protein expression. 5-Aza administration 24 h after coal and silica exposure significantly inhibited pneumoconiosis [45].…”

Section: Thymocyte Differentiation Antigen 1 (Thy-1)mentioning

confidence: 89%

More than a Genetic Code: Epigenetics of Lung Fibrosis

et al. 2020

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At the end of the last century, genetic studies reported that genetic information is not transmitted solely by DNA, but is also transmitted by other mechanisms, named as epigenetics. The well-described epigenetic mechanisms include DNA methylation, biochemical modifications of histones, and microRNAs. The role of altered epigenetics in the biology of various fibrotic diseases is well-established, and recent advances demonstrate its importance in the pathogenesis of pulmonary fibrosis—predominantly referring to idiopathic pulmonary fibrosis, the most lethal of the interstitial lung diseases. The deficiency in effective medications suggests an urgent need to better understand the underlying pathobiology. This review summarizes the current knowledge concerning epigenetic changes in pulmonary fibrosis and associations of these changes with several cellular pathways of known significance in its pathogenesis. It also designates the most promising substances for further research that may bring us closer to new therapeutic options.

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“…Dust exposure can induce hypermethylation of Thy-1 DNA in RLE-6TN cells and in rats. Pretreatment of RLE-6TN cells and rats with the DNMT inhibitor 5-aza-2′-deoxycytidine (5-aza-dC) can reduce the fibrosis [ 36 ]. In a trans-well culture model of rat primary alveolar macrophages and rat primary lung fibroblasts by Hou and Li et al [ 37 – 39 ], DNA methylation levels of a large number of genes were altered during the SiO 2 -induced fibroblast to myofibroblast progression.…”

Section: Dna Methylationmentioning

confidence: 99%

Epigenetic Changes and Functions in Pneumoconiosis

Cheng

Fan

et al. 2022

Oxidative Medicine and Cellular Longevity

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Pneumoconiosis is one of the most common occupational diseases in the world, and specific treatment methods of pneumoconiosis are lacking at present, so it carries great social and economic burdens. Pneumoconiosis, coronavirus disease 2019, and idiopathic pulmonary fibrosis all have similar typical pathological changes—pulmonary fibrosis. Pulmonary fibrosis is a chronic lung disease characterized by excessive deposition of the extracellular matrix and remodeling of the lung tissue structure. Clarifying the pathogenesis of pneumoconiosis plays an important guiding role in its treatment. The occurrence and development of pneumoconiosis are accompanied by epigenetic factors (e.g., DNA methylation and noncoding RNA) changes, which in turn can promote or inhibit the process of pneumoconiosis. Here, we summarize epigenetic changes and functions in the several kinds of evidence classification (epidemiological investigation, in vivo, and in vitro experiments) and main types of cells (macrophages, fibroblasts, and alveolar epithelial cells) to provide some clues for finding specific therapeutic targets for pneumoconiosis and even for pulmonary fibrosis.

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Dust induces lung fibrosis through dysregulated DNA methylation

Cited by 26 publications

References 58 publications

Idiopathic Pulmonary Fibrosis: An Update on Pathogenesis

Idiopathic Pulmonary Fibrosis: An Update on Pathogenesis

More than a Genetic Code: Epigenetics of Lung Fibrosis

Epigenetic Changes and Functions in Pneumoconiosis

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