Trial reportThe Journal of biological chemistry2014
Asbestos-induced disruption of calcium homeostasis induces endoplasmic reticulum stress in macrophages.
Trial report in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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
28 citing papers in PubMed, 44 citations in OpenAlex.
- Preparation methodology evaluation of rat pulmonary tissues containing mineral fibers following inhalation exposure to Libby amphibole asbestos.Journal of occupational medicine and toxicology (London, England) · 2025Article
- The PERK/ATF4 pathway is required for metabolic reprogramming and progressive lung fibrosis.JCI insight · 2025Article
- The Effects of Endoplasmic Reticulum Stress via Intratracheal Instillation of Water-Soluble Acrylic Acid Polymer on the Lungs of Rats.International journal of molecular sciences · 2024Article
- Effects of Natural Products through Inhibiting Endoplasmic Reticulum Stress on Attenuation of Idiopathic Pulmonary Fibrosis.Drug design, development and therapy · 2024Review
- Understanding the impact of ER stress on lung physiology.Frontiers in cell and developmental biology · 2024Review
- Asbestos and Iron.International journal of molecular sciences · 2023Review
- Pharmacological targeting of endoplasmic reticulum stress in disease.Nature reviews. Drug discovery · 2022Review
- Selenoprotein K deficiency-induced apoptosis: A role for calpain and the ERS pathway.Redox biology · 2021Article
- Oxidative Stress and Endoplasmic Reticulum Stress in Rare Respiratory Diseases.Journal of clinical medicine · 2021Review
- Centrality of Myeloid-Lineage Phagocytes in Particle-Triggered Inflammation and Autoimmunity.Frontiers in toxicology · 2021Review
- Increased Levels of ER Stress and Apoptosis in a Sheep Model for Pulmonary Fibrosis Are Alleviated byCanadian respiratory journal · 2021Article
- Role of unfolded proteins in lung disease.Thorax · 2021Review
- Mitochondrial quality control in pulmonary fibrosis.Redox biology · 2020Review
- The P5-type ATPase Spf1 is required for development and virulence of the rice blast fungus Pyricularia oryzae.Current genetics · 2020Article
- Targeting Calcium Signalling in Malignant Mesothelioma.Cancers · 2019Review
- Mitochondrial calcium uniporter regulates PGC-1α expression to mediate metabolic reprogramming in pulmonary fibrosis.Redox biology · 2019Article
- Heme scavenging reduces pulmonary endoplasmic reticulum stress, fibrosis, and emphysema.JCI insight · 2018Observational
- Exosomes from asbestos-exposed cells modulate gene expression in mesothelial cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Endoplasmic reticulum stress in pulmonary fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- The Secretory Response of Rat Peritoneal Mast Cells on Exposure to Mineral Fibers.International journal of environmental research and public health · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Although the mechanisms for fibrosis development remain largely unknown, recent evidence indicates that endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) may act as an important fibrotic stimulus in diseased lungs. ER stress is observed in lungs of patients with idiopathic pulmonary fibrosis. In this study we evaluated if ER stress and the UPR was present in macrophages exposed to chrysotile asbestos and if ER stress in macrophages was associated with asbestos-induced pulmonary fibrosis. Macrophages exposed to chrysotile had elevated transcript levels of several ER stress genes. Macrophages loaded with the Ca(2+)-sensitive dye Fura2-AM showed that cytosolic Ca(2+) increased significantly within minutes after chrysotile exposure and remained elevated for a prolonged time. Chrysotile-induced increases in cytosolic Ca(2+) were partially inhibited by either anisomycin, an inhibitor of passive Ca(2+) leak from the ER, or 1,2-bis(2-aminophenoxyl)ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM), an intracellular Ca(2+) chelator known to deplete ER Ca(2+) stores. Anisomycin inhibited X-box-binding protein 1 (XBP1) mRNA splicing and reduced immunoglobulin-binding protein (BiP) levels, whereas BAPTA-AM increased XBP1 splicing and BiP expression, suggesting that ER calcium depletion may be one factor contributing to ER stress in cells exposed to chrysotile. To evaluate ER stress in vivo, asbestos-exposed mice showed fibrosis development, and alveolar macrophages from fibrotic mice showed increased expression of BiP. Bronchoalveolar macrophages from asbestosis patients showed increased expression of several ER stress genes compared with normal subjects. These findings suggest that alveolar macrophages undergo ER stress, which is associated with fibrosis development.
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Registered trials
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.