ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
Modulation of reactive oxygen species by Rac1 or catalase prevents asbestos-induced pulmonary fibrosis.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 85 citations in OpenAlex.
- Asbestos-induced disruption of calcium homeostasis induces endoplasmic reticulum stress in macrophages.The Journal of biological chemistry · 2014Trial
- The Mechanism of Oxidative Stress in Pulmonary Fibrosis and Research Progress.Antioxidants (Basel, Switzerland) · 2026Review
- Investigation of the protective effect of cilostazol on acute lung injury-mediated inflammation and in silico molecular modelling studies of inflammatory signalling pathway: a repurposing study.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- The PERK/ATF4 pathway is required for metabolic reprogramming and progressive lung fibrosis.JCI insight · 2025Article
- The role of oxidative stress-related genes in idiopathic pulmonary fibrosis.Scientific reports · 2025Article
- Macrophage Immunometabolism in Pulmonary Homeostasis and Chronic Lung Diseases.International journal of biological sciences · 2025Review
- Sex and disease regulate major histocompatibility complex class I expression in human lung epithelial cells.Physiological reports · 2024Article
- NADPH Oxidase 3: Beyond the Inner Ear.Antioxidants (Basel, Switzerland) · 2024Review
- Emerging delivery approaches for targeted pulmonary fibrosis treatment.Advanced drug delivery reviews · 2024Review
- Contribution of Mitochondrial Reactive Oxygen Species to Chronic Hypoxia-Induced Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2023Article
- Effect of the new silicon-based agent on the symptoms of interstitial pneumonitis.Scientific reports · 2023Article
- Secretome of hESC-Derived MSC-like Immune and Matrix Regulatory Cells Mitigate Pulmonary Fibrosis through Antioxidant and Anti-Inflammatory Effects.Biomedicines · 2023Article
- DOCK2 contributes to pulmonary fibrosis by promoting lung fibroblast to myofibroblast transition.American journal of physiology. Cell physiology · 2022Article
- eNAMPT Is a Novel Damage-associated Molecular Pattern Protein That Contributes to the Severity of Radiation-induced Lung Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- Molecular hydrogen is a promising therapeutic agent for pulmonary disease.Journal of Zhejiang University. Science. B · 2022Article
- Role of Molecular Hydrogen in Ageing and Ageing-Related Diseases.Oxidative medicine and cellular longevity · 2022Review
- The interplay of DAMPs, TLR4, and proinflammatory cytokines in pulmonary fibrosis.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Targeting Oxidative Stress as a Therapeutic Approach for Idiopathic Pulmonary Fibrosis.Frontiers in pharmacology · 2021Review
- Cadmium-mediated lung injury is exacerbated by the persistence of classically activated macrophages.The Journal of biological chemistry · 2020Article
- Increased Lung Catalase Activity Confers Protection Against Experimental RSV Infection.Scientific reports · 2020Article
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 4 institutions in 2 countries.
Funding
Abstract
The release of reactive oxygen species (ROS) and cytokines by alveolar macrophages has been demonstrated in asbestos-induced pulmonary fibrosis, but the mechanism linking alveolar macrophages to the pathogenesis is not known. The GTPase Rac1 is a second messenger that plays an important role in host defense. In this study, we demonstrate that Rac1 null mice are protected from asbestos-induced pulmonary fibrosis, as determined by histological and biochemical analysis. We hypothesized that Rac1 induced pulmonary fibrosis via generation of ROS. Asbestos increased TNF-alpha and ROS in a Rac1-dependent manner. TNF-alpha was elevated only 1 day after exposure, whereas ROS generation progressively increased in bronchoalveolar lavage cells obtained from wild-type (WT) mice. To determine whether ROS generation contributed to pulmonary fibrosis, we overexpressed catalase in WT monocytes and observed a decrease in ROS generation in vitro. More importantly, administration of catalase to WT mice attenuated the development of fibrosis in vivo. For the first time, these results demonstrate that Rac1 plays a crucial role in asbestos-induced pulmonary fibrosis. Moreover, it suggests that a simple intervention may be useful to prevent progression of the disease.
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.