ArticleVeterinary sciences2022
Minute Cellular Nodules as Early Lesions in Rats with Silica Exposure via Inhalation.
Article in Veterinary sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Inhibition of PADI2-mediated vimentin citrullination alleviates silica-induced pulmonary fibrosis in mice.Particle and fibre toxicology · 2026Article
- Targeting the Secretin Receptor in Macrophages Attenuates Silica-Induced Pulmonary Fibrosis.Cell proliferation · 2025Article
- Targeting Lp-PLA2 inhibits profibrotic monocyte-derived macrophages in silicosis through restoring cardiolipin-mediated mitophagy.Cellular & molecular immunology · 2025Article
- Effect of macrophage-to-myofibroblast transition on silicosis.Animal models and experimental medicine · 2025Article
- Quercetin Alleviates Pulmonary Fibrosis in Silicotic Mice by Inhibiting Macrophage Transition and TGF-β-Smad2/3 Pathway.Current issues in molecular biology · 2023Article
- Effect of Sex Differences in Silicotic Mice.International journal of molecular sciences · 2022Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Mechanisms of silicosis have yet to be clarified, and pathological conditions are inaccurately described in some experimental studies on silicosis. This study was aimed at describing initial lesions in silicosis, as observed in rats with silica exposure via inhalation, and major histopathologic alterations. Male Wistar rats were exposed to silica for 24 weeks. Hematoxylin and eosin staining indicated the presence of "cellular nodule+ macrophage alveolitis" in rats exposed to silica from the 2-16 weeks time points and "fibrotic cellular + cellular nodule" in rats exposed to silica via inhalation for 24 weeks. By immunohistochemistry, the following were noted: a continual increase in the positive expression of CD68 in macrophages in the lungs of rats exposed to silica; hyperplasia in alveolar type II cells (AT2); loss of original phenotypes in fibrotic cellular nodules, macrophages, and AT2 cells; loss of endothelial cells in silicotic nodules; and positive expression of α-smooth muscle actin in macrophages. Typical pathological changes in silicosis were also summarized. Among these changes were macrophage alveolitis, cellular nodules, and fibrotic cellular nodules, including an increase in minute cellular nodules in the early stages and the formation of fibrotic cellular nodules in the late stages.
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