ArticlePloS one2010
Reactive oxygen species are required for maintenance and differentiation of primary lung fibroblasts in idiopathic pulmonary fibrosis.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
What it found
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Who cites it
83 citing papers in PubMed, 146 citations in OpenAlex.
- Matrices of physiologic stiffness potently inactivate idiopathic pulmonary fibrosis fibroblasts.American journal of respiratory cell and molecular biology · 2013Trial
- Engineered Lecithin-Polymer Hybrid Micelles for Enhanced Gallic Acid Delivery: Response Surface Optimization and Preclinical Evaluation.AAPS PharmSciTech · 2026Article
- Paclitaxel-eluting silicone airway stent with sustained drug release and potent anti-fibrotic activity.Frontiers in bioengineering and biotechnology · 2026Article
- Pathological Interplay of ROS With Myofibroblasts: An Impediment to Corneal Restitution.Oxidative medicine and cellular longevity · 2026Review
- αCGRP deficiency aggravates pulmonary fibrosis by promoting senescence in alveolar type 2 cells.Genes and immunity · 2025Article
- Celastrol-Ligustrazine compound proven to be a novel drug candidate for idiopathic pulmonary fibrosis by intervening in the TGF-β1 mediated pathways-an experimental in vitro and vivo study.Molecular diversity · 2025Article
- Survival impact and safety comparison of pirfenidone and nintedanib for idiopathic pulmonary fibrosis: A meta-analysis.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2025Article
- Mechanisms and markers of lung ageing in health and disease.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Iron metabolism in rheumatic diseases.Journal of translational autoimmunity · 2025Review
- Deciphering the Correlation between the Emergence of Lung Carcinoma Associated with Tuberculosis-related Inflammation.Endocrine, metabolic & immune disorders drug targets · 2025Review
- Mechanistic role for mTORC1 signaling in profibrotic toxicity of low-dose cadmium.Toxicology and applied pharmacology · 2025Article
- Idiopathic Pulmonary Fibrosis: Review of Current Knowledge.Physiological research · 2024Review
- NADPH Oxidase 3: Beyond the Inner Ear.Antioxidants (Basel, Switzerland) · 2024Review
- Therapeutic potential of melatonin in targeting molecular pathways of organ fibrosis.Pharmacological reports : PR · 2024Review
- Genome-wide RNA sequencing of ocular fibroblasts from glaucomatous and normal eyes: Implications for glaucoma management.PloS one · 2024Article
- Transformation of macrophages into myofibroblasts in fibrosis-related diseases: emerging biological concepts and potential mechanism.Frontiers in immunology · 2024Review
- Passage dependence of NADH redox status and reactive oxygen species levelTranslational breast cancer research : a journal focusing on translational research in breast cancer · 2024Article
- Macrophages and fibroblasts in foreign body reactions: How mechanical cues drive cell functions?Materials today. Bio · 2023Review
- Small-molecule-mediated OGG1 inhibition attenuates pulmonary inflammation and lung fibrosis in a murine lung fibrosis model.Nature communications · 2023Article
- The telomerase activator TA-65 protects from cigarette smoke-induced small airway remodeling in mice through extra-telomeric effects.Scientific reports · 2023Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIdiopathic pulmonary fibrosis (IPF) is a progressive and fatal illness whose pathogenesis remains poorly understood. Recent evidence suggests oxidative stress as a key player in the establishment/progression of lung fibrosis in animal models and possibly in human IPF. The aim of the present study was to characterize the cellular phenotype of fibroblasts derived from IPF patients and identify underlying molecular mechanisms. METHODOLOGY/PRINCIPAL
findingsWe first analyzed the baseline differentiation features and growth ability of primary lung fibroblasts derived from 7 histology proven IPF patients and 4 control subjects at different culture passages. Then, we focused on the redox state and related molecular pathways of IPF fibroblasts and investigated the impact of oxidative stress in the establishment of the IPF phenotype. IPF fibroblasts were differentiated into alpha-smooth muscle actin (SMA)-positive myofibroblasts, displayed a pro-fibrotic phenotype as expressing type-I collagen, and proliferated lower than controls cells. The IPF phenotype was inducible upon oxidative stress in control cells and was sensitive to ROS scavenging. IPF fibroblasts also contained large excess of reactive oxygen species (ROS) due to the activation of an NADPH oxidase-like system, displayed higher levels of tyrosine phosphorylated proteins and were more resistant to oxidative-stress induced cell death. Interestingly, the IPF traits disappeared with time in culture, indicating a transient effect of the initial trigger. CONCLUSIONS/SIGNIFICANCE: Robust expression of α-SMA and type-I collagen, high and uniformly-distributed ROS levels, resistance to oxidative-stress induced cell death and constitutive activation of tyrosine kinase(s) signalling are distinctive features of the IPF phenotype. We suggest that this phenotype can be used as a model to identify the initial trigger of IPF.
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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.