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
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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“Likewise inflammatory responses are observed after exposure to other particulates such as found in diesel exhaust (5).”
From Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica (2008) · cites this paper as [5]
In the citing paper
“The inhalation and deposition of particulate pollutants, such as diesel exhaust, asbestos, or silica, in the small airways is known to induce inflammatory responses leading to sustained inflammation, lung fibrosis, and cancer (22, 25).”
From Volcanic Ash Activates the NLRP3 Inflammasome in Murine and Human Macrophages (2018) · cites this paper as [25]
In the citing paper
“IL-1 cytokines are potent mediators of innate immunity in response to crystalline silica exposure (23, 24) and have been implicated in the pathophysiology of human and experimental diseases (25, 26).”
From Volcanic Ash Activates the NLRP3 Inflammasome in Murine and Human Macrophages (2018) · cites this paper as [25]
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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
- Published
- 2005-03
- Volume
- 11
- Issue
- 2
- Pages
- 169-173
- ISSN
- 1070-5287 (ISSN-L)
- 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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