ArticlePloS one2015
Plasminogen activator inhibitor-1 in cigarette smoke exposure and influenza A virus infection-induced lung injury.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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
20 citing papers in PubMed, 43 citations in OpenAlex.
- Review
- Elevated plasma level of PAI-1 is associated with severe COVID-19.Scientific reports · 2025Article
- Vitronectin regulates lung tissue remodeling and emphysema in chronic obstructive pulmonary disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Caveolin-1-derived peptide attenuates cigarette smoke-induced airway and alveolar epithelial injury.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- CSE reduces OTUD4 triggering lung epithelial cell apoptosis via PAI-1 degradation.Cell death & disease · 2023Article
- Review
- Divergent Regulation of Alveolar Type 2 Cell and Fibroblast Apoptosis by Plasminogen Activator Inhibitor 1 in Lung Fibrosis.The American journal of pathology · 2021Article
- Astragalin Inhibits Cigarette Smoke-Induced Pulmonary Thrombosis and Alveolar Inflammation and Disrupts PAR Activation and Oxidative Stress-Responsive MAPK-Signaling.International journal of molecular sciences · 2021Article
- Redox control in the pathophysiology of influenza virus infection.BMC microbiology · 2020Review
- Acute Lung Injury: IL-17A-Mediated Inflammatory Pathway and Its Regulation by Curcumin.Inflammation · 2019Review
- Changes in the expression level of IL-17A and p53-fibrinolytic system in smokers with or without COPD.Molecular biology reports · 2018Article
- PAI-1 gain-of-function genotype, factors increasing PAI-1 levels, and airway obstruction: The GALA II Cohort.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2017Article
- Regulation of p53-mediated changes in the uPA-fibrinolytic system and in lung injury by loss of surfactant protein C expression in alveolar epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- p53 and miR-34a Feedback Promotes Lung Epithelial Injury and Pulmonary Fibrosis.The American journal of pathology · 2017Article
- SERPINE1 -844 and -675 polymorphisms and chronic obstructive pulmonary disease in a Chinese Han population.The Journal of international medical research · 2016Article
- Plasminogen activator inhibitor-1 does not contribute to the pulmonary pathology induced by acute exposure to ozone.Physiological reports · 2016Article
- Aberrant coagulation causes a hyper-inflammatory response in severe influenza pneumonia.Cellular & molecular immunology · 2016Review
- The vitronectin RGD motif regulates TGF-β-induced alveolar epithelial cell apoptosis.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- p53- and PAI-1-mediated induction of C-X-C chemokines and CXCR2: importance in pulmonary inflammation due to cigarette smoke exposure.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Elevated circulating PAI-1 levels are related to lung function decline, systemic inflammation, and small airway obstruction in chronic obstructive pulmonary disease.International journal of chronic obstructive pulmonary disease · 2016Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Parenchymal lung inflammation and airway and alveolar epithelial cell apoptosis are associated with cigarette smoke exposure (CSE), which contributes to chronic obstructive pulmonary disease (COPD). Epidemiological studies indicate that people exposed to chronic cigarette smoke with or without COPD are more susceptible to influenza A virus (IAV) infection. We found increased p53, PAI-1 and apoptosis in AECs, with accumulation of macrophages and neutrophils in the lungs of patients with COPD. In Wild-type (WT) mice with passive CSE (PCSE), p53 and PAI-1 expression and apoptosis were increased in AECs as was lung inflammation, while those lacking p53 or PAI-1 resisted AEC apoptosis and lung inflammation. Further, inhibition of p53-mediated induction of PAI-1 by treatment of WT mice with caveolin-1 scaffolding domain peptide (CSP) reduced PCSE-induced lung inflammation and reversed PCSE-induced suppression of eosinophil-associated RNase1 (EAR1). Competitive inhibition of the p53-PAI-1 mRNA interaction by expressing p53-binding 3'UTR sequences of PAI-1 mRNA likewise suppressed CS-induced PAI-1 and AEC apoptosis and restored EAR1 expression. Consistent with PCSE-induced lung injury, IAV infection increased p53, PAI-1 and apoptosis in AECs in association with pulmonary inflammation. Lung inflammation induced by PCSE was worsened by subsequent exposure to IAV. Mice lacking PAI-1 that were exposed to IAV showed minimal viral burden based on M2 antigen and hemagglutination analyses, whereas transgenic mice that overexpress PAI-1 without PCSE showed increased M2 antigen and inflammation after IAV infection. These observations indicate that increased PAI-1 expression promotes AEC apoptosis and exacerbates lung inflammation induced by IAV following PCSE.
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Registered trials
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