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Cited by 326Occupational and environmental lung diseasesInterstitial Lung Diseases and Idiopathic Pulmonary FibrosisSarcoidosis and Beryllium Toxicity Research

The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.

Basic pathogenetic mechanisms in silicosis: current understanding

Rimal, Binaya, Greenberg, Alissa K, Rom, William N·2005·Current Opinion in Pulmonary Medicine
DOI 10.1097/01.mcp.0000152998.11335.24
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Abstract

PURPOSE OF REVIEW: Silicosis continues to be a common cause of chronic lung diseases, despite evidence that these diseases can be prevented by environmental dust control. Silicosis has been studied extensively by basic and clinical scientists, yet little is known about the crucial cellular and molecular mechanisms that initiate and propagate the process of inflammation and scarring. RECENT FINDINGS: Recent in vivo, in vitro, and human studies have focused on several main areas of investigation into the causes and processes of the development of silicosis. These areas of investigation include the variability of pathogenic potential of different varieties of silica; the role of activated alveolar macrophages products in the development and progression of silicosis; and the direct role played by the silica particle surface in triggering adverse biologic reactions, such as generating ROS and RNS. The generation of oxidants by silica particles and by silica-activated cells results in cell and lung damage; increased expression of inflammatory cytokines, including TNF-alpha, IL 1 beta, and TGF-beta; activation of cell signaling pathways, including the MAP kinase pathways; and phosphorylation and activation of specific transcription factors (e.g., NFkB). The ROS, RNS, and NO generated by the silica particles also induce apoptosis in macrophages and other cells. SUMMARY: Further research on the molecular mechanisms involved in the inflammatory processes important for progression to fibrotic diseases is needed for the development of effective treatment of silicosis. Potential therapeutic strategies include inhibition of cytokines such as IL-1, TNF alpha, the use of anti-oxidants, and the inhibition of apoptosis.

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Crossref · 10.1097/01.mcp.0000152998.11335.24

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Research works printed but not linked: 8

  1. Working, 1997, Monogr Eval Carcinog Risks Hum, 68, 1
  2. Sherson, 1990, J Occup Med, 32, 110
  3. Watanabe, 1987, J Clin Lab Immunol, 23, 45
  4. Davis, 1998, J Environ Pathol Toxicol Oncol, 17, 99
  5. Davis, 1998, J Environ Pathol Toxicol Oncol, 17, 99
  6. Barbarin, 2004, Am J Respir Crit Care Med, 31, 78
  7. Zhang, 1999, Am J Physiol, 277, 743
  8. Iyer, 1996, Toxicol Appl Pharmacol, 141, 84, 10.1016/S0041-008X(96)80012-3 · DOI

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Metadata

Authors
Rimal, B., Greenberg, A. K., & Rom, W. N.
Affiliations
NYU Langone Health (US)
Corresponding author
Greenberg, Alissa K
ORCID
Rom, William N
Venue
Current Opinion in Pulmonary Medicine
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2005-03
Volume
11
Issue
2
Pages
169-173
ISSN
1070-5287 (ISSN-L)
DOI
10.1097/01.mcp.0000152998.11335.24
OpenAlex
W2116650911
Cited by
326
References
38
Citations by year
2026: 2 · 2025: 13 · 2024: 13 · 2023: 21 · 2022: 20 · 2021: 17 · 2020: 14 · 2019: 19 · 2018: 19 · 2017: 14 · 2016: 13 · 2015: 22 · 2014: 15 · 2013: 17 · 2012: 13
FWCI
2.70
Type
journal article
Language
en
Open access
closed
Locations
  • Current Opinion in Pulmonary Medicine (publishedVersion)
  • PubMed (publishedVersion)
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
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Sarcoidosis and Beryllium Toxicity Research
Keywords
silicosis, silica, alveolar macrophages, reactive oxygen species, reactive nitrogen species, oxidative stress, inflammation, pulmonary fibrosis, cytokines, MAPK signaling, NF-κB, apoptosis, antioxidant therapy, cytokine inhibition
MeSH terms
Animals, Disease Models, Animal, Humans, Lung, Necrosis, Phagocytosis, Silicon Dioxide, Silicosis, Oxidative Stress, Mice, Rats

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