Asbestos-induced lung diseases: an update.

Asbestos-induced lung diseases: an update.
复制标题

石棉引起的肺部疾病:更新。

DOI:
10.1016/j.trsl.2009.01.004
复制
发表时间:
2009-04
期刊:
Translational research : the journal of laboratory and clinical medicine
影响因子:
--
通讯作者:
Kamp DW
Kamp DW
中科院分区:
其他
文献类型:
--
作者:
Kamp DW

文献摘要

参考文献

被引文献

相似文献

石棉通过尚未完全阐明的机制引起石棉沉滞症(石棉吸入引起的肺纤维化)和恶性肿瘤(支气管癌和间皮瘤)。尽管世界范围内石棉使用量大幅减少,但石棉引起的肺部疾病仍然是一个重大的健康问题,主要是因为在20世纪世纪期间开采、加工和使用了大量的纤维,加上暴露和疾病表现之间长达40年的潜伏期。本文综述了过去几年中出现的重要的新流行病学和病原学信息。虽然石棉肺的发展与石棉暴露的程度和持续时间直接相关,但恶性细胞克隆的发展可能发生在低水平石棉暴露的情况下。重点放在最近的流行病学调查,探讨发生恶性肿瘤的风险,从非职业性,环境石棉暴露。越来越多的研究揭示了石棉损害肺的新机制途径。注意力集中在肺泡上皮细胞(AEC)的损伤和修复的重要性,铁衍生的活性氧(ROS)的作用,和凋亡的p53和p53调节的死亡途径。此外,最近的证据强调了调节细胞因子和生长因子产生的特定细胞信号传导途径的关键作用。上皮间质转化(EMT)的不断发展的作用也进行了审查。这些研究的转化意义是显而易见的,为开发石棉相关肺部疾病的新治疗策略提供了分子基础,重要的是,其他肺部疾病,如间质性肺纤维化和肺癌。
Asbestos causes asbestosis (pulmonary fibrosis caused by asbestos inhalation) and malignancies (bronchogenic carcinoma and mesothelioma) by mechanisms that are not fully elucidated. Despite a dramatic reduction in asbestos use worldwide, asbestos-induced lung diseases remain a substantial health concern primarily because of the vast amounts of fibers that have been mined, processed, and used during the 20th century combined with the long latency period of up to 40 years between exposure and disease presentation. This review summarizes the important new epidemiologic and pathogenic information that has emerged over the past several years. Whereas the development of asbestosis is directly associated with the magnitude and duration of asbestos exposure, the development of a malignant clone of cells can occur in the setting of low-level asbestos exposure. Emphasis is placed on the recent epidemiologic investigations that explore the malignancy risk that occurs from nonoccupational, environmental asbestos exposure. Accumulating studies are shedding light on novel mechanistic pathways by which asbestos damages the lung. Attention is focused on the importance of alveolar epithelial cell (AEC) injury and repair, the role of iron-derived reactive oxygen species (ROS), and apoptosis by the p53- and mitochondria-regulated death pathways. Furthermore, recent evidence underscores crucial roles for specific cellular signaling pathways that regulate the production of cytokines and growth factors. An evolving role for epithelial-mesenchymal transition (EMT) is also reviewed. The translational significance of these studies is evident in providing the molecular basis for developing novel therapeutic strategies for asbestos-related lung diseases and, importantly, other pulmonary diseases, such as interstitial pulmonary fibrosis and lung cancer.
DOI: 10.1074/jbc.m709273200
发表时间: 2008-03-07
影响因子: 4.8
作者:
Gao, Fei;Koenitzer, Jeffrey R.;Oury, Tim D.
通讯作者: Oury, Tim D.
DOI: 10.1136/bmj.2.3491.1024
发表时间: 1927-07-01
影响因子: 105.7
作者:
Cooke, WE
通讯作者: Cooke, WE
DOI: 10.1093/carcin/bgm090
发表时间: 2007-09-01
期刊: CARCINOGENESIS
影响因子: 4.7
作者:
Aung, Winn;Hasegawa, Sumitaka;Saga, Tsuneo
通讯作者: Saga, Tsuneo
DOI: 10.1016/j.mrgentox.2008.06.011
发表时间: 2008-08-01
影响因子: 1.9
作者:
Amati, Monica;Tomasetti, Marco;Santarelli, Lory
通讯作者: Santarelli, Lory
DOI: 10.1126/science.1156995
发表时间: 2008-05-02
期刊: SCIENCE
影响因子: 56.9
作者:
Dostert, Catherine;Petrilli, Virginie;Tschopp, Jurg
通讯作者: Tschopp, Jurg