ReviewToxicological sciences : an official journal of the Society of Toxicology2019
Role of Macrophages in Acute Lung Injury and Chronic Fibrosis Induced by Pulmonary Toxicants.
Review in Toxicological sciences : an official journal of the Society of Toxicology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers, 1 of them a synthesis that pooled it.
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Who cites it
137 citing papers in PubMed, 1 synthesis or guideline pooled it, 276 citations in OpenAlex.
- Mechanism and clinical application of ozone therapy in treating skin ulcer diseases.Medical gas research · 2026Pooled it
- Macrophage polarization plasticity in pulmonary fibrosis: a review from pathogenesis to therapeutic targeting.Inflammopharmacology · 2026Review
- BCL9 inhibition promotes fibroblast lipogenesis by regulating macrophage-fibroblast interactions to attenuate pulmonary fibrosis.Signal transduction and targeted therapy · 2026Article
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- Pulmonary fibrosis: Emerging targets and novel therapeutics.The Journal of international medical research · 2026Review
- The CaInternational journal of molecular sciences · 2026Article
- The dynamic landscape of alternative splicing during silicosis progression.Respiratory research · 2026Article
- Lung injury, oxidative stress, and impaired functioning in a model of prolonged ozone exposure in female mice are associated with macrophage proinflammatory and profibrotic activation and altered bioenergetics.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Micro- and Nanoplastics and Pulmonary Health: The Current State of Research.Microplastics (Basel, Switzerland) · 2026Article
- Rus-GXF, a ruscogenin glycoside, binds to the ADP-binding domain of JAK1 to prevent inflammation and barrier damage in acute lung injury.Frontiers in pharmacology · 2026Article
- Macrophage Phenotypic Plasticity and Inflammatory Mechanisms in Hyperoxia-Induced Lung Injury.Journal of inflammation research · 2026Review
- Disulfiram Attenuates Bleomycin-Induced Lung Inflammation and Fibrosis with Reduced Endothelial Pyroptosis and Neutrophil Adhesion.Journal of inflammation research · 2026Article
- Voacangine mitigates lipopolysaccharide-produced sepsis-triggered acute lung injury via inhibition of PERK/PI3K and TLR4/NF-кB/IL-1β pathways in mice.Journal of molecular histology · 2025Article
- IGF1R deficiency mitigates acute lung injury by promoting anti-inflammatory transcriptional profiles.Respiratory research · 2025Article
- Harpagide Confers Protection Against Acute Lung Injury Through Multi-Omics Dissection of Immune-Microenvironmental Crosstalk and Convergent Therapeutic Mechanisms.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Radiation-induced Lung Injury (RILI) in Non-human Primates (NHPs) Induces Cellular Senescence and Upregulation of Tyrosine Kinase Fgr, which is Detectable in Bronchoalveolar Lavage.Radiation research · 2025Article
- Mouse mesenchymal stem cell-derived exosomal miR-205-5p modulates LPS-induced macrophage polarization and alleviates lung injury by regulating the USP7/FOXM1 axis.Drug delivery and translational research · 2025Article
- Lipopolysaccharide induces retention of E-cadherin in the endoplasmic reticulum and promotes hybrid epithelial-to-mesenchymal transition of human embryonic stem cells-derived expandable lung epithelial cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Connective Tissue Disorder-Induced Diffuse Alveolar Hemorrhage: A Comprehensive Review with an Emphasis on Airway and Respiratory Management.Life (Basel, Switzerland) · 2025Review
- Review
77 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A diverse group of toxicants has been identified that cause injury to the lung including gases (eg, ozone, chlorine), particulates/aerosols (eg, diesel exhaust, fly ash, other combustion products, mustards, nanomaterials, silica, asbestos), chemotherapeutics (eg, bleomycin), and radiation. The pathologic response to these toxicants depends on the dose and duration of exposure and their physical/chemical properties. A common response to pulmonary toxicant exposure is an accumulation of proinflammatory/cytotoxic M1 macrophages at sites of tissue injury, followed by the appearance of anti-inflammatory/wound repair M2 macrophages. It is thought that the outcome of the pathogenic responses to toxicants depends on the balance in the activity of these macrophage subpopulations. Overactivation of either M1 or M2 macrophages leads to injury and disease pathogenesis. Thus, the very same macrophage-derived mediators, released in controlled amounts to destroy injurious materials and pathogens (eg, reactive oxygen species, reactive nitrogen species, proteases, tumor necrosis factor α) and initiate wound repair (eg, transforming growth factor β, connective tissue growth factor, vascular endothelial growth factor), can exacerbate acute lung injury and/or induce chronic disease such as fibrosis, chronic obstructive pulmonary disease, and asthma, when released in excess. This review focuses on the role of macrophage subsets in acute lung injury and chronic fibrosis. Understanding how these pathologies develop following exposure to toxicants, and the contribution of resident and inflammatory macrophages to disease pathogenesis may lead to the development of novel approaches for treating lung diseases.
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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.