The DOI matches its Crossref record; 109 of the 111 references it cites were found in a registry or an index.
Asbestos-induced lung diseases: an update
Open accessAbstract
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.
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“Iron ions were considered to play a key role in asbestos toxicity because of their ability to catalyse generation of reactive oxygen species (ROS)5–7.”
From Surface reactivity of amphibole asbestos: a comparison between crocidolite and tremolite (2017) · cites this paper as [6]
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“In asbestos toxicology, iron-generated free radicals are largely held as one of the causes of asbestos malignant effect.”
From Surface reactivity of amphibole asbestos: a comparison between crocidolite and tremolite (2017) · cites this paper as [6]
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Cites
Defining the role of mTOR in cancer
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Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica
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Advances in Malignant Mesothelioma
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Mechanisms in the Pathogenesis of Asbestosis and Silicosis
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Balkwill, F. R. (2006) · Cancer and Metastasis Reviews · doi:10.1007/s10555-006-9005-3 · Cited by 919
The Nalp3 inflammasome is essential for the development of silicosis
Cassel, S. L., Eisenbarth, S. C., Iyer, S. S., Sadler, J. J., Colegio, O. R., Tephly, L. A., Carter, A. B., Rothman, P. B., Flavell, R. A., & Sutterwala, F. S. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0803933105 · Cited by 907
Fibroblasts Derive from Hepatocytes in Liver Fibrosis via Epithelial to Mesenchymal Transition
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The inflammasome: a danger sensing complex triggering innate immunity
Pétrilli, V., Dostert, C., Muruve, D. A., & Tschopp, J. (2007) · Current Opinion in Immunology · doi:10.1016/j.coi.2007.09.002 · Cited by 700
The genetics of the p53 pathway, apoptosis and cancer therapy
Vázquez, A., Bond, E. E., Levine, A. J., & Bond, G. L. (2008) · Nature Reviews Drug Discovery · doi:10.1038/nrd2656 · Cited by 686
Flagged first, then by citations
2 of the 111 references couldn’t be matched to a known paper.
Research works printed but not linked: 1
- Kamp, 2002, Asbestos-associated cancers: clinical spectrum and pathogenic mechanisms, Clin Occup Environ Med, 2, 753, 10.1016/S1526-0046(03)00023-2 · DOI
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Germline BAP1 Mutations Predispose to Malignant Mesothelioma
Testa, J. R., Cheung, M., Pei, J., Below, J. E., Tan, Y., Sementino, E., Cox, N. J., Dogan, A. U., Pass, H. I., Trusa, S., et al. (2011) · Nature Genetics · doi:10.1038/ng.912 · Cited by 1,076
Fleischner Society: Glossary of Terms for Thoracic Imaging
Bankier, A. A., MacMahon, H., Colby, T. V., Gevenois, P. A., Goo, J. M., Leung, A. N. C., Lynch, D. A., Schaefer‐Prokop, C. M., Tomiyama, N., Travis, W. D., et al. (2024) · Radiology · doi:10.1148/radiol.232558 · Cited by 438
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Pulmonary toxicity of carbon nanotubes and asbestos — Similarities and differences
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Inflammation and immune surveillance in cancer
Chow, M. T., Möller, A., & Smyth, M. J. (2011) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2011.12.004 · Cited by 253
Metadata
- Authors
- Kamp, D. W.
- Affiliations
- Northwestern University (US)
- Corresponding author
- Kamp, David W.
- Venue
- Translational Research
- Publisher
- Elsevier BV
- Published
- 2009-04
- Volume
- 153
- Issue
- 4
- Pages
- 143-152
- ISSN
- 1878-1810 (ISSN-L)
- 1931-5244
- PMC
- PMC3544481
- OpenAlex
- W2115450306
- Cited by
- 251
- References
- 111
- Citations by year
- 2026: 4 · 2025: 12 · 2024: 11 · 2023: 17 · 2022: 9 · 2021: 17 · 2020: 12 · 2019: 12 · 2018: 10 · 2017: 11 · 2016: 6 · 2015: 15 · 2014: 22 · 2013: 27 · 2012: 22
- FWCI
- 3.27
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Translational research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL035440)
- National Institute of Environmental Health Sciences (R01ES013995)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Occupational and environmental lung diseases
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Social Sciences › Health › Occupational Health and Global Justice
- Keywords
- asbestos, asbestosis, pulmonary fibrosis, mesothelioma, lung cancer, asbestos exposure, environmental asbestos exposure, alveolar epithelial cells, reactive oxygen species, iron, apoptosis, p53, mitochondrial apoptosis, cytokines, growth factors, epithelial-mesenchymal transition, interstitial pulmonary fibrosis, latency period, pathogenesis
- MeSH terms
- Asbestos, Humans, Lung Diseases
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