期刊
ANNUAL REVIEW OF PATHOLOGY: MECHANISMS OF DISEASE, VOL 8
卷 8, 期 -, 页码 161-187出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-pathol-020712-163942
关键词
asbestosis; epithelium; mitochondria; OGG1; aconitase; p53
类别
资金
- NIEHS NIH HHS [R01 ES020357, R01ES020357] Funding Source: Medline
- BLRD VA [I01 BX000786] Funding Source: Medline
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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