Molecular basis of asbestos-induced lung disease.
Molecular basis of asbestos-induced lung disease.
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DOI：
10.1146/annurev-pathol-020712-163942
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发表时间：
2013-01-24
期刊：
影响因子：
--
通讯作者：
Kamp DW
中科院分区：
文献类型：
--
作者：
Liu G;Cheresh P;Kamp DW
石棉引起石棉沉着病和恶性肿瘤的分子机制尚未完全了解。石棉沉滞症、肺癌和间皮瘤的潜在作用模式似乎因纤维类型、肺清除率和遗传学而异。在回顾了石棉暴露后的关键病理变化后，我们研究了最近发现的致病途径，重点是氧化应激。肺泡上皮细胞凋亡是石棉肺重要的早期事件，由线粒体和p53调节的死亡途径介导，并可能受到内质网的调节。我们回顾线粒体DNA（mtDNA）的损伤和修复机制，重点是8-氧代鸟嘌呤DNA糖基化酶，以及活性氧产生，mtDNA损伤，p53，OGG 1，和线粒体顺乌头酸酶之间的串扰。这些对石棉诱导的肺部疾病的分子基础的新见解可能促进用于管理退行性疾病的新治疗靶点的开发（例如，石棉肺和特发性肺纤维化）、肿瘤和衰老，缺乏有效的管理。
Asbestos causes asbestosis and malignancies by molecular mechanisms that are not fully understood. The modes of action underlying asbestosis, lung cancer, and mesothelioma appear to differ depending on the fiber type, lung clearance, and genetics. After reviewing the key pathologic changes following asbestos exposure, we examine recently identified pathogenic pathways, with a focus on oxidative stress. Alveolar epithelial cell apoptosis, which is an important early event in asbestosis, is mediated by mitochondria- and p53-regulated death pathways and may be modulated by the endoplasmic reticulum. We review mitochondrial DNA (mtDNA)-damage and -repair mechanisms, focusing on 8-oxoguanine DNA glycosylase, as well as cross talk between reactive oxygen species production, mtDNA damage, p53, OGG1, and mitochondrial aconitase. These new insights into the molecular basis of asbestos-induced lung diseases may foster the development of novel therapeutic targets for managing degenerative diseases (e.g., asbestosis and idiopathic pulmonary fibrosis), tumors, and aging, for which effective management is lacking.
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DOI：
10.1164/ajrccm.151.5.7735593
发表时间：
1995-05-01
影响因子：
24.7
作者：
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通讯作者：
STEVENS, B
影响因子：
2.9
作者：
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11.5
作者：
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影响因子：
5.3
作者：
Bacsi, Attila;Chodaczek, Grzegorz;Boldogh, Istvan
通讯作者：
Boldogh, Istvan
DOI：
10.1084/jem.20102049
发表时间：
2011-03-14
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Bulua AC;Simon A;Maddipati R;Pelletier M;Park H;Kim KY;Sack MN;Kastner DL;Siegel RM
通讯作者：
Siegel RM