ArticleMolecular medicine (Cambridge, Mass.)2021
The antioxidant N-acetylcysteine promotes immune response and inhibits epithelial-mesenchymal transition to alleviate pulmonary fibrosis in chronic obstructive pulmonary disease by suppressing the VWF/p38 MAPK axis.
Article in Molecular medicine (Cambridge, Mass.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- p38 MAPK signaling in chronic obstructive pulmonary disease pathogenesis and inhibitor therapeutics.Cell communication and signaling : CCS · 2023Pooled it
- miR-214-3p Mediates Samarium Oxide-Induced Pulmonary Fibrosis by Targeting MAP2K3 via the MAPK Signaling Pathway.Toxics · 2026Article
- Oxidative stress-associated genes TPPP3 and VEGFA in COPD revealed by bulk and single-cell sequencing analysis.Scientific reports · 2026Article
- Butyrate Regulating Inflammatory Responses in Chronic Obstructive Pulmonary Disease via the Gut-Lung Axis.International journal of chronic obstructive pulmonary disease · 2026Review
- Sodium butyrate targets VWF to inhibit cigarette smoke extract-induced endothelial cell-macrophage crosstalk in regulating inflammatory response.Respiratory research · 2025Article
- Antioxidants and Reactive Oxygen Species: Shaping Human Health and Disease Outcomes.International journal of molecular sciences · 2025Review
- Epithelial Cell Dysfunction in Pulmonary Fibrosis: Mechanisms, Interactions, and Emerging Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Current Understanding of Pulmonary Fibrosis: Pathogenesis, Diagnosis, and Therapeutic Approaches.Canadian respiratory journal · 2025Review
- Mitochondria-target ubiquinone attenuates bleomycin-induced pulmonary fibrosis.Frontiers in pharmacology · 2025Article
- Therapeutic Potential of N-acetylcysteine and Glycine in Reducing Pulmonary Injury in Diabetic Rats.Cureus · 2024Article
- Nrf2 mediates the effects of shionone on silica-induced pulmonary fibrosis.Chinese medicine · 2024Article
- Cigarette Smoke Extract Induces MUC5AC Expression Through the ROS/ IP3R/CaInternational journal of chronic obstructive pulmonary disease · 2024Article
- Asarinin attenuates bleomycin-induced pulmonary fibrosis by activating PPARγ.Scientific reports · 2023Article
- Advances in the Use ofAntioxidants (Basel, Switzerland) · 2023Review
- Novel Key Ingredients in Urinary Tract Health-The Role of D-mannose, Chondroitin Sulphate, Hyaluronic Acid, andNutrients · 2023Review
- Epithelial-Mesenchymal Transition Mechanisms in Chronic Airway Diseases: A Common Process to Target?International journal of molecular sciences · 2023Review
- Transaldolase inhibits CD36 expression by modulating glutathione-p38 signaling, exerting protective effects against macrophage foam cell formation.Acta biochimica et biophysica Sinica · 2023Article
- CXCL17 Attenuates Diesel Exhaust Emissions Exposure-Induced Lung Damage by Regulating Macrophage Function.Toxics · 2023Article
- Intraperitoneal BromAcCancers · 2023Article
- N-Acetylcysteine Administration Improves the Redox and Functional Gene Expression Levels in Spleen, Mesenteric Lymph Node and Gastrocnemius Muscle in Piglets Infected with Porcine Epidemic Diarrhea Virus.Animals : an open access journal from MDPI · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimN-Acetylcysteine (NAC) demonstrates applications in the prevention of exacerbation of chronic obstructive pulmonary disease (COPD). COPD is often characterized by fibrosis of the small airways. This study aims at investigating the physiological mechanisms by which NAC might mediate the pulmonary fibrosis in COPD.
methodsA total of 10 non-smokers without COPD and 10 smokers with COPD were recruited in this study, and COPD rat models were established. Cigarette smoke extract (CSE) cell models were constructed. The gain- or loss-of-function experiments were adopted to determine the expression of VWF and the extent of p38 MAPK phosphorylation, levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and immunoglobulins (IgG, IgM and IgA) in the serum of COPD rats and supernatant of alveolar epithelial cells and to detect cell invasion and migration and the ratio of CD3
resultsExpression of VWF and the extent of p38 MAPK phosphorylation were increased in COPD. NAC inhibited p38 MAPK phosphorylation by reducing the VWF expression. NAC could inhibit cell migration and invasion, elevate E-cadherin expression, the ratio of CD3
conclusionsCollectively, NAC could ameliorate COPD-induced pulmonary fibrosis by promoting immune response and inhibiting EMT process via the VWF/p38 MAPK axis, therefore providing us with a potential therapeutic target for treating COPD.
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