Trial reportScientific reports2019
Lipid Uptake by Alveolar Macrophages Drives Fibrotic Responses to Silica Dust.
Trial report in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 59 citations in OpenAlex.
- The metabolic code of pulmonary disease: from mechanisms to therapeutic opportunities.Breathe (Sheffield, England) · 2026Review
- Chronic IL-21 exposure reshapes pulmonary environment, elevating risk of respiratory diseases.Cellular and molecular life sciences : CMLS · 2026Article
- SSO targets CD36 to regulate lipid metabolism disorders and improve SiOCurrent research in toxicology · 2026Article
- The impact of macrophage metabolism on idiopathic pulmonary fibrosis development and treatment prospectives.Frontiers in immunology · 2026Review
- Cholesterol-mediated inflammation activation in alveolar macrophages.BMC biology · 2025Article
- Phospholipid composition in small airway lining fluid among tunnel construction workers exposed to respirable crystalline silica.Lipids in health and disease · 2025Article
- Silicosis: from pathogenesis to therapeutics.Frontiers in pharmacology · 2025Review
- Characterization of prostate macrophage heterogeneity, foam cell markers, and CXCL17 upregulation in a mouse model of steroid hormone imbalance.Scientific reports · 2024Article
- Macrophage Polarization and Functions in Pathogenesis of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2024Review
- PROSTATE CELL HETEROGENEITY AND CXCL17 UPREGULATION IN MOUSE STEROID HORMONE IMBALANCE.bioRxiv : the preprint server for biology · 2024Article
- Spatial transcriptomics reveals alterations in perivascular macrophage lipid metabolism in the onset of Wooden Breast myopathy in broiler chickens.Scientific reports · 2024Article
- CD36/Lyn kinase interactions within macrophages promotes pulmonary fibrosis in response to oxidized phospholipid.Respiratory research · 2023Article
- The Multifaceted Role of Osteopontin in Prostate Pathologies.Biomedicines · 2023Review
- Novel lipidomes profile and clinical phenotype identified in pneumoconiosis patients.Journal of health, population, and nutrition · 2023Article
- Steroid hormone imbalance drives macrophage infiltration and Spp1/osteopontinThe Journal of pathology · 2023Article
- Airway macrophages display decreased expression of receptors mediating and regulating scavenging in early cystic fibrosis lung disease.Frontiers in immunology · 2023Article
- Lipidomics Profiles and Lipid Metabolite Biomarkers in Serum of Coal Workers' Pneumoconiosis.Toxics · 2022Article
- Excess iron promotes emergence of foamy macrophages that overexpress ferritin in the lungs of silicosis patients.Respirology (Carlton, Vic.) · 2022Article
- Editorial: Host immune evasion byFrontiers in immunology · 2022Article
- Role of metabolic reprogramming in pro-inflammatory cytokine secretion from LPS or silica-activated macrophages.Frontiers in immunology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Silicosis is a common occupational disease and represents a significant contributor to respiratory morbidity and mortality worldwide. Lipid-laden macrophages, or foam cells, are observed in the lungs of patients with silicosis but the mechanisms mediating their formation remain poorly understood. In this study, we sought to elucidate the mechanisms by which silica promotes foam cell formation in the lung, and to determine whether uptake of lipids alone is sufficient to drive TGF-β production by alveolar macrophages. Consistent with previous reports, we found that foam cells were markedly increased in the lungs of patients with silicosis and that these findings associated with both higher levels of intracellular lipid levels (oxidized LDL, ox-LDL) and elevated transcript levels for the lipid scavenger receptor CD36 and the nuclear receptor PPARγ. Employing a rat alveolar macrophage cell line, we found that exposure to silica dust or ox-LDL alone had a modest effect on the induction of foam cell formation and only silica was capable of inducing the production of TGF-β. In contrast, foam cell formation and TGF-β production were both dramatically increased when cells were exposed to a combination of silica dust and ox-LDL. Moreover, we found that these endpoints were markedly attenuated by either blocking CD36 or inhibiting the activity of PPARγ. Altogether, our findings suggest that foam cell formation and TGF-β production are driven by the simultaneous uptake of silica and lipids in alveolar macrophages and that strategies aimed at blocking lipid uptake by alveolar macrophages might be effective in ameliorating fibrotic responses to silica in the lung.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.