ArticleJournal of immunology (Baltimore, Md. : 1950)2014
TNFR1/phox interaction and TNFR1 mitochondrial translocation Thwart silica-induced pulmonary fibrosis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 37 citations in OpenAlex.
- Article
- Role of macrophage ATP metabolism disorder in SiOPurinergic signalling · 2025Review
- A comprehensive retrospect on the current perspectives and future prospects of pneumoconiosis.Frontiers in public health · 2024Review
- Crystalline silica-induced proinflammatory eicosanoid storm in novel alveolar macrophage model quelled by docosahexaenoic acid supplementation.Frontiers in immunology · 2023Article
- Role of metabolic reprogramming in pro-inflammatory cytokine secretion from LPS or silica-activated macrophages.Frontiers in immunology · 2022Review
- Metabolic Adaptation of Macrophages as Mechanism of Defense against Crystalline Silica.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- The Mechanism and Effect of Autophagy, Apoptosis, and Pyroptosis on the Progression of Silicosis.International journal of molecular sciences · 2021Review
- Atractylenolide III alleviates the apoptosis through inhibition of autophagy by the mTOR-dependent pathway in alveolar macrophages of human silicosis.Molecular and cellular biochemistry · 2021Article
- NADPH Oxidase Inhibition in Fibrotic Pathologies.Antioxidants & redox signaling · 2020Article
- Role of Nephronectin in Pathophysiology of Silicosis.International journal of molecular sciences · 2019Review
- Dioscin Alleviates Crystalline Silica-Induced Pulmonary Inflammation and Fibrosis through Promoting Alveolar Macrophage Autophagy.Theranostics · 2019Article
- An updated review of the genotoxicity of respirable crystalline silica.Particle and fibre toxicology · 2018Review
- A Pathological Study of Acute Pulmonary Toxicity Induced by Inhaled Kanto Loam Powder.International journal of molecular sciences · 2018Article
- circHIPK2-mediated σ-1R promotes endoplasmic reticulum stress in human pulmonary fibroblasts exposed to silica.Cell death & disease · 2017Article
- BBC3 in macrophages promoted pulmonary fibrosis development through inducing autophagy during silicosis.Cell death & disease · 2017Article
- LASSBio-897 Reduces Lung Injury Induced by Silica Particles in Mice: Potential Interaction with the AFrontiers in pharmacology · 2017Article
- Macrophage-derived MCPIP1 mediates silica-induced pulmonary fibrosis via autophagy.Particle and fibre toxicology · 2016Article
- MCPIP1 Regulates Alveolar Macrophage Apoptosis and Pulmonary Fibroblast Activation After in vitro Exposure to Silica.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Neutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease.Nature medicine · 2016Article
- TRPV4 Mechanosensitive Ion Channel Regulates Lipopolysaccharide-Stimulated Macrophage Phagocytosis.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Macrophages play a fundamental role in innate immunity and the pathogenesis of silicosis. Phagocytosis of silica particles is associated with the generation of reactive oxygen species (ROS), secretion of cytokines, such as TNF, and cell death that contribute to silica-induced lung disease. In macrophages, ROS production is executed primarily by activation of the NADPH oxidase (Phox) and by generation of mitochondrial ROS (mtROS); however, the relative contribution is unclear, and the effects on macrophage function and fate are unknown. In this study, we used primary human and mouse macrophages (C57BL/6, BALB/c, and p47(phox-/-)) and macrophage cell lines (RAW 264.7 and IC21) to investigate the contribution of Phox and mtROS to silica-induced lung injury. We demonstrate that reduced p47(phox) expression in IC21 macrophages is linked to enhanced mtROS generation, cardiolipin oxidation, and accumulation of cardiolipin hydrolysis products, culminating in cell death. mtROS production is also observed in p47(phox-/-) macrophages, and p47(phox-/-) mice exhibit increased inflammation and fibrosis in the lung following silica exposure. Silica induces interaction between TNFR1 and Phox in RAW 264.7 macrophages. Moreover, TNFR1 expression in mitochondria decreased mtROS production and increased RAW 264.7 macrophage survival to silica. These results identify TNFR1/Phox interaction as a key event in the pathogenesis of silicosis that prevents mtROS formation and reduces macrophage apoptosis.
Indexed as
Identifiers
What OpenQuestion holds
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.