ArticleThe American journal of pathology2005
Carbon monoxide suppresses bleomycin-induced lung fibrosis.
Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.
- The bleomycin animal model: a useful tool to investigate treatment options for idiopathic pulmonary fibrosis?The international journal of biochemistry & cell biology · 2008Pooled it
- Islet Harvest in Carbon Monoxide-Saturated Medium for Chronic Pancreatitis Patients Undergoing Islet Autotransplantation.Cell transplantation · 2019Trial
- Low Dose Carbon Monoxide Exposure in Idiopathic Pulmonary Fibrosis Produces a CO Signature Comprised of Oxidative Phosphorylation Genes.Scientific reports · 2019Trial
- A Phase II Clinical Trial of Low-Dose Inhaled Carbon Monoxide in Idiopathic Pulmonary Fibrosis.Chest · 2018Trial
- Elucidating the Molecular Pathways and Therapeutic Interventions of Gaseous Mediators in the Context of Fibrosis.Antioxidants (Basel, Switzerland) · 2024Review
- The effect of extracorporeal shock wave on joint capsule fibrosis based on AJournal of orthopaedic surgery and research · 2023Article
- Carbon monoxide (CO) derived from the CO-releasing molecule CORM-2 reduces peritoneal adhesion formation in a rat model.Molecular biology reports · 2023Article
- Heme Oxygenase-1: An Anti-Inflammatory Effector in Cardiovascular, Lung, and Related Metabolic Disorders.Antioxidants (Basel, Switzerland) · 2022Review
- Heme Oxygenase 1 in Vertebrates: Friend and Foe.Cell biochemistry and biophysics · 2022Review
- Nuclear respiratory factor-1 negatively regulates TGF-β1 and attenuates pulmonary fibrosis.iScience · 2022Article
- Gasotransmitters: Potential Therapeutic Molecules of Fibrotic Diseases.Oxidative medicine and cellular longevity · 2021Review
- Mitochondrial dysfunction in lung ageing and disease.European respiratory review : an official journal of the European Respiratory Society · 2020Review
- Carbon monoxide in intensive care medicine-time to start the therapeutic application?!Intensive care medicine experimental · 2020Review
- Formation of high molecular weight p62 by CORM-3.PloS one · 2019Article
- Hydrogen Sulfide: A Therapeutic Option in Systemic Sclerosis.International journal of molecular sciences · 2018Review
- Carbon monoxide in lung cell physiology and disease.American journal of physiology. Cell physiology · 2018Review
- Role of Platelet-Derived Transforming Growth Factor-β1 and Reactive Oxygen Species in Radiation-Induced Organ Fibrosis.Antioxidants & redox signaling · 2017Review
- Delivery of Antioxidant and Anti-inflammatory Agents for Tissue Engineered Vascular Grafts.Frontiers in pharmacology · 2017Review
- Article
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis is an incurable fibrosing disorder that progresses relentlessly to respiratory failure. We hypothesized that a product of heme oxygenase activity, carbon monoxide (CO), may have anti-fibrotic effects. To test this hypothesis, mice treated with intratracheal bleomycin were exposed to low-concentration inhaled CO or ambient air. Lungs of mice treated with CO had significantly lower hydroxyproline accumulation than controls. Fibroblast proliferation, thought to play a central role in the progression of fibrosis, was suppressed by in vitro exposure to CO. CO caused increased cellular levels of p21(Cip1) and decreased levels of cyclins A and D. This effect was independent of the observed suppression of MAPK's phosphorylation by CO but was dependent on increased cGMP levels. Further, CO-exposed cells elaborated significantly less fibronectin and collagen-1 than control cells. This same effect was seen in vivo. Suppression of collagen-1 production did not depend on MAPK or guanylate cyclase signaling pathways but did depend on the transcriptional regulator Id1. Taken together, these data suggest that CO exerts an anti-fibrotic effect in the lung, and this effect may be due to suppression of fibroblast proliferation and/or suppression of matrix deposition by fibroblasts.
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.