Association of Environmental Pollutants Exposure with Pulmonary Fibrosis: A Mini Review of Molecular Mechanism Mediated

Soni Siswanto, B. W. Wardhani
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引用次数: 1

Abstract

Pulmonary fibrosis is a specific form of chronic progressive interstitial lung disease. Deposition of extracellular matrix, mainly collagen, is the pathogenic characteristic of pulmonary fibrosis. Many reports show that environmental pollutants, particularly asbestos, silica, mercury, cadmium, and benzo(a)pyrene, are contributed in the etiology of lung injury and a risk factor in the development of idiopathic pulmonary fibrosis (IPF) in humans. Based on its physicochemical properties, environmental pollutant-induced pulmonary fibrosis can be developed after a particular type or dose of exposure. To date, some studies have focused on variant pollutants that are induced. However, the molecular mechanism of various pollutants to cause lung injury, which leads to pulmonary fibrosis, remained unexplored. Hence, this narrative review articles describe its molecular mechanism in generating pulmonary fibrosis comprehensively. It is helpful to portray the IPF pathogenesis and its drug discovery and development. Collectively, this article also revealed animal models which can be useful for IPF drug development research.
环境污染物暴露与肺纤维化的关系——介导的分子机制综述
肺纤维化是慢性进行性间质性肺病的一种特殊形式。细胞外基质沉积,主要是胶原沉积,是肺纤维化的致病特征。许多报告表明,环境污染物,特别是石棉、二氧化硅、汞、镉和苯并(a)芘,是肺损伤的病因之一,也是人类特发性肺纤维化(IPF)发展的危险因素。根据其物理化学性质,环境污染物诱导的肺纤维化可以在特定类型或剂量的暴露后发展。到目前为止,一些研究集中在诱发的变异污染物上。然而,各种污染物引起肺损伤,从而导致肺纤维化的分子机制尚未探索。因此,这篇叙述性综述文章全面描述了其在肺纤维化发生中的分子机制。这有助于描述IPF的发病机制及其药物的发现和开发。总之,本文还揭示了可用于IPF药物开发研究的动物模型。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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