ArticleOncotarget2017
Melatonin suppresses fibrotic responses induced by cigarette smoke via downregulation of TGF-β1.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Pooled it
- Endoplasmic reticulum stress and the unfolded protein response in lung diseases: molecular pathways and therapeutic interventions.The Journal of pathology · 2026Review
- Melatonin attenuates inflammation, remodeling, and oxidative stress in experimental models of asthma and COPD.Frontiers in immunology · 2026Article
- [Mechanism of melatonin regulating the expression level of rhythm genes to alleviate interstitial pulmonary fibrosis].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2024Article
- Therapeutic effects of melatonin on the lungs of rats exposed to passive smoking.Respiratory research · 2024Article
- Therapeutic potential of melatonin in targeting molecular pathways of organ fibrosis.Pharmacological reports : PR · 2024Review
- Protective effects of inhaled antioxidants against air pollution-induced pathological responses.Respiratory research · 2023Review
- Recent Advances (2015-2020) in Drug Discovery for Attenuation of Pulmonary Fibrosis and COPD.Molecules (Basel, Switzerland) · 2023Review
- Role of melatonin in respiratory diseases (Review).Experimental and therapeutic medicine · 2022Review
- The Involvement of PDE4 in the Protective Effects of Melatonin on Cigarette-Smoke-Induced Chronic Obstructive Pulmonary Disease.Molecules (Basel, Switzerland) · 2021Article
- Melatonin as a Potential Adjuvant Treatment for COVID-19 beyond Sleep Disorders.International journal of molecular sciences · 2021Review
- Article
- A nutraceutical strategy for downregulating TGFβ signalling: prospects for prevention of fibrotic disorders, including post-COVID-19 pulmonary fibrosis.Open heart · 2021Article
- Targeting Oxidative Stress as a Therapeutic Approach for Idiopathic Pulmonary Fibrosis.Frontiers in pharmacology · 2021Review
- Melatonin down-regulates steroidal hormones, thymocyte apoptosis and inflammatory cytokines in middle-aged T. cruzi infected rats.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- Targeting Aging Pathways in Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2020Review
- Cellular stress responses and dysfunctional Mitochondrial-cellular senescence, and therapeutics in chronic respiratory diseases.Redox biology · 2020Review
- Effects of Exogenous Melatonin on MAM Induced Lung Injury and Lung Development in Mice Offspring.Tanaffos · 2020Article
- Article
- What Range of Motion and Functional Results Can Be Expected After Open Arthrolysis with Hinged External Fixation For Severe Posttraumatic Elbow Stiffness?Clinical orthopaedics and related research · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cigarette smoke (CS) is the most important risk factor in the development of chronic obstructive pulmonary disease (COPD). Pulmonary fibrosis is an irreversible response and important feature of COPD. In this study, we investigated the effects of melatonin on fibrotic response in development of COPD using a CS and lipopolysaccharide (LPS) induced COPD model and cigarette smoke condensate (CSC)-stimulated NCI-H292 cells, a human mucoepidermoid cell line. Mice were exposed to CS for 1 h per day (8 cigarettes per day) from day 1 to day 7 and were treated intranasally with LPS on day 4. Melatonin (10 or 20 mg/kg) was injected intraperitoneally 1 h before CS exposure. Melatonin decreased the inflammatory cell counts in bronchoalveolar lavage fluid (BALF), with a reduction in transforming growth factor (TGF)-β1. Melatonin inhibited the expression of TGF-β1, collagen I and SMAD3 phosphorylation in lung tissue exposed to CS and LPS. In CSC-stimulated H292 cells, melatonin suppressed the elevated expression of fibrotic mediators induced by CSC treatment. Melatonin reduced the expression of TGF-β1, collagen I, SMAD3 and p38 phosphorylation in CSC-stimulated H292 cells. In addition, cotreatment with melatonin and TGF-β1 inhibitors significantly limited fibrotic mediators, with greater reductions in the expression of TGF-β1, collagen I, SMAD3 and p38 phosphorylation than those of H292 cells treated with TGF-β1 inhibitor alone. Taken together, melatonin effectively inhibited fibrotic responses induced by CS and LPS exposure, which was related to the downregulation of TGF-β1. Therefore, our results suggest that melatonin may suppress the pulmonary fibrotic response induced by CS.
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Registered trials
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