Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (574 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A form of pneumoconiosis resulting from inhalation of dust containing crystalline form of silicon dioxide, usually in the form of quartz. Amorphous silica is relatively nontoxic.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Silicoses.
Where it fits in the MeSH classification
- Broader topics
- Pneumoconiosis
- Narrower topics
- Anthracosilicosis; Silicotuberculosis
Related concepts
- Silicon Dioxide
Research landscape
PubMed indexes 8,398 records tagged with the MeSH heading “Silicosis” (counts retrieved 2026-11-04). 881 of them (10.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 6,144 records.
Reviews account for 406 records (4.8%) and meta-analyses for 23. Randomized controlled trials number 30 (0.4%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 6,144 |
| 2000-2009 | 634 |
| 2010-2019 | 739 |
| 2020 onward | 881 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 406 | 4.8% |
| Meta-analyses | 23 | 0.3% |
| Randomized controlled trials | 30 | 0.4% |
Method: PubMed query "Silicosis"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in respiratory medicine
Research on airway and lung disease mixes lung-function tests, symptom diaries, imaging and hospital records, so what was measured and in whom matters as much as the result. Many conditions here, such as asthma and COPD, vary between people and over time, and exposure studies (smoking, pollution, workplace dust) show association rather than proof of cause. Nothing on this page is advice about treatment or inhalers; anyone with breathing difficulty should seek care from a qualified clinician. Check how the condition was defined, the severity of the people studied and whether outcomes were symptoms, lung function or hospital admissions.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Mesenchymal stem cells use extracellular vesicles to outsource mitophagy and shuttle microRNAs | 2015 | Research article Design not recorded in structured metadata | 877 | cc by PMID 26442449 · DOI · PMC4598952 |
| New Insights into Pathomechanisms and Treatment Possibilities for Lung Silicosis | 2021 | Review article Design not recorded in structured metadata | 143 | cc by PMID 33920534 · DOI · PMC8072896 |
| Pyroptosis in inflammation-related respiratory disease | 2022 | Review article Design not recorded in structured metadata | 140 | cc by PMID 35819638 · DOI · PMC9684248 |
| Macrophage-Derived Ferritin Exacerbates Silica-Induced Pulmonary Fibrosis via PIK3R2-Mediated Fibroblast Differentiation | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 41566645 · DOI · PMC13042690 |
Mesenchymal stem cells use extracellular vesicles to outsource mitophagy and shuttle microRNAs [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Mesenchymal stem cells (MSCs) and macrophages are fundamental components of the stem cell niche and function coordinately to regulate haematopoietic stem cell self-renewal and mobilization.
- Closing excerpt
- Collectively, these studies mechanistically link mitophagy and MSC survival with macrophage function, thereby providing a physiologically relevant context for the innate immunomodulatory activity of MSCs.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (144 words)
Mesenchymal stem cells (MSCs) and macrophages are fundamental components of the stem cell niche and function coordinately to regulate haematopoietic stem cell self-renewal and mobilization. Recent studies indicate that mitophagy and healthy mitochondrial function are critical to the survival of stem cells, but how these processes are regulated in MSCs is unknown. Here we show that MSCs manage intracellular oxidative stress by targeting depolarized mitochondria to the plasma membrane via arrestin domain-containing protein 1-mediated microvesicles. The vesicles are then engulfed and re-utilized via a process involving fusion by macrophages, resulting in enhanced bioenergetics. Furthermore, we show that MSCs simultaneously shed micro RNA-containing exosomes that inhibit macrophage activation by suppressing Toll-like receptor signalling, thereby de-sensitizing macrophages to the ingested mitochondria. Collectively, these studies mechanistically link mitophagy and MSC survival with macrophage function, thereby providing a physiologically relevant context for the innate immunomodulatory activity of MSCs.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26442449 · DOI · PMC4598952
New Insights into Pathomechanisms and Treatment Possibilities for Lung Silicosis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Inhalation of silica particles is an environmental and occupational cause of silicosis, a type of pneumoconiosis.
- Closing excerpt
- This article reviews new information on the pathophysiology of silicosis and points out several promising treatment approaches targeting silicosis-related pathways.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (104 words)
Inhalation of silica particles is an environmental and occupational cause of silicosis, a type of pneumoconiosis. Development of the lung silicosis is a unique process in which the vicious cycle of ingestion of inhaled silica particles by alveolar macrophages and their release triggers inflammation, generation of nodular lesions, and irreversible fibrosis. The pathophysiology of silicosis is complex, and interactions between the pathomechanisms have not been completely understood. However, elucidation of silica-induced inflammation cascades and inflammation-fibrosis relations has uncovered several novel possibilities of therapeutic targeting. This article reviews new information on the pathophysiology of silicosis and points out several promising treatment approaches targeting silicosis-related pathways.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33920534 · DOI · PMC8072896
Pyroptosis in inflammation-related respiratory disease [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Pyroptosis is commonly induced by the gasdermin (GSDM) family and is accompanied by the release of inflammatory cytokines such as IL-1β and IL-18.
- Closing excerpt
- In conclusion, pyroptosis may play a role in inflammation-related respiratory diseases, providing new therapeutic targets.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (173 words)
Pyroptosis is commonly induced by the gasdermin (GSDM) family and is accompanied by the release of inflammatory cytokines such as IL-1β and IL-18. Recently, increasing evidence suggests that pyroptosis plays a role in respiratory diseases. This review aimed to summarize the roles and mechanisms of pyroptosis in inflammation-related respiratory diseases. There are several pathways involved in pyroptosis, such as the canonical inflammasome-induced pathway, non-canonical inflammasome-induced pathway, caspase-1/3/6/7/GSDMB pathway, caspase-8/GSDMC pathway, caspase-8/GSDMD pathway, and caspase-3/GSEME pathway. Pyroptosis may be involved in asthma, chronic obstructive pulmonary disease (COPD), lung cancer, acute lung injury (ALI), silicosis, pulmonary hypertension (PH), and tuberculosis (TB), in which the NLRP3 inflammasome-induced pathway is mostly highlighted. Pyroptosis contributes to the deterioration of asthma, COPD, ALI, silicosis, and PH. In addition, pyroptosis has dual effects on lung cancer and TB. Additionally, whether pyroptosis participates in cystic fibrosis (CF) and sarcoidosis or not is largely unknown, though the activation of NLRP3 inflammasome is found in CF and sarcoidosis. In conclusion, pyroptosis may play a role in inflammation-related respiratory diseases, providing new therapeutic targets.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35819638 · DOI · PMC9684248
Macrophage-Derived Ferritin Exacerbates Silica-Induced Pulmonary Fibrosis via PIK3R2-Mediated Fibroblast Differentiation [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Silicosis is a progressive and life-threatening fibrotic lung disease caused by crystalline silica.
- Closing excerpt
- These findings underscore that ferritin functions not only as a potential clinical biomarker for silicosis surveillance but also as a pathogenic driver through macrophage-fibroblast crosstalk, and provide a theoretical foundation for developing integrated diagnostic and therapeutic strategies against silicosis.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (153 words)
Silicosis is a progressive and life-threatening fibrotic lung disease caused by crystalline silica. However, targeted therapies remain unavailable due to its incompletely understood pathogenic mechanisms. Here, we identify ferritin as a pivotal mediator of silica-induced pulmonary fibrosis by integrating clinical exploration with experimental validation. We detected persistently elevated ferritin levels in lung tissues and serum from silicosis patients and silica-exposed mice, and demonstrated that exogenous ferritin administration exacerbates fibrosis in vivo. Multi-omics profiling and co-culture experiments revealed that macrophage-secreted ferritin promotes fibroblast-to-myofibroblast differentiation and pathological extracellular matrix (ECM) deposition via the PIK3R2/SMAD signaling axis. Importantly, genetic knockdown of ferritin in macrophages significantly suppressed myofibroblast differentiation and collagen accumulation both in vivo and in vitro. These findings underscore that ferritin functions not only as a potential clinical biomarker for silicosis surveillance but also as a pathogenic driver through macrophage-fibroblast crosstalk, and provide a theoretical foundation for developing integrated diagnostic and therapeutic strategies against silicosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41566645 · DOI · PMC13042690
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Silicosis [5]
- Research article Mechanisms in the pathogenesis of asbestosis and silicosis [6]
- Research article Silica-related diseases in the modern world [7]
- Research article Silica-associated lung disease: An old-world exposure in modern industries [8]
- Research article Basic pathogenetic mechanisms in silicosis: current understanding [9]
- Research article Health hazards due to the inhalation of amorphous silica [10]
References
- Phinney DG, Di Giuseppe M, Njah J, Sala E, Shiva S, St Croix CM, et al.. Mesenchymal stem cells use extracellular vesicles to outsource mitophagy and shuttle microRNAs. . 2015. PMID 26442449 · DOI · PMC4598952
- Adamcakova J, Mokra D. New Insights into Pathomechanisms and Treatment Possibilities for Lung Silicosis. . 2021. PMID 33920534 · DOI · PMC8072896
- Feng Y, Li M, Yangzhong X, Zhang X, Zu A, Hou Y, et al.. Pyroptosis in inflammation-related respiratory disease. . 2022. PMID 35819638 · DOI · PMC9684248
- Wang L, Chen X, Quan H, Qian R, Gong S, He Q, et al.. Macrophage-Derived Ferritin Exacerbates Silica-Induced Pulmonary Fibrosis via PIK3R2-Mediated Fibroblast Differentiation. . 2026. PMID 41566645 · DOI · PMC13042690
- Leung CC, Yu IT, Chen W. Silicosis. Lancet. 2012. PMID 22534002 · DOI
- Mossman BT, Churg A. Mechanisms in the pathogenesis of asbestosis and silicosis. Am J Respir Crit Care Med. 1998. PMID 9603153 · DOI
- Hoy RF, Chambers DC. Silica-related diseases in the modern world. Allergy. 2020. PMID 31989662 · DOI
- Barnes H, Goh NSL, Leong TL, Hoy R. Silica-associated lung disease: An old-world exposure in modern industries. Respirology. 2019. PMID 31517432 · DOI
- Rimal B, Greenberg AK, Rom WN. Basic pathogenetic mechanisms in silicosis: current understanding. Curr Opin Pulm Med. 2005. PMID 15699791 · DOI
- Merget R, Bauer T, Küpper HU, Philippou S, Bauer HD, Breitstadt R, et al.. Health hazards due to the inhalation of amorphous silica. Arch Toxicol. 2002. PMID 11876495 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.