ArticleInternational journal of chronic obstructive pulmonary disease
Increased matrix metalloproteinase-9 to tissue inhibitor of metalloproteinase-1 ratio in smokers with airway hyperresponsiveness and accelerated lung function decline.
Article in International journal of chronic obstructive pulmonary disease. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- p38 MAPK signaling in chronic obstructive pulmonary disease pathogenesis and inhibitor therapeutics.Cell communication and signaling : CCS · 2023Pooled it
- AhR as a Common Denominator in Immunity and Inflammation in Chronic Lung Diseases: Molecular and Clinical Insights.Diseases (Basel, Switzerland) · 2026Review
- Differential proteomic analysis of lung tissues in rats with high-altitude pulmonary edema and screening of potential biomarkers.Frontiers in physiology · 2026Article
- Environmental Arsenic Exposure, Biomarkers and Lung Function in Children from Yaqui Communities in Sonora, Mexico.Journal of xenobiotics · 2025Article
- Article
- IL-6 and TIMP-1 Correlated to Airway Pathogen Colonization and Predict Disease Severity in Patients with Non-Cystic Fibrosis Bronchiectasis.Journal of inflammation research · 2024Article
- Tissue Inhibitor of Matrix Metalloproteinases-1 (TIMP-1) and Pulmonary Involvement in COVID-19 Pneumonia.Biomolecules · 2023Article
- TIMP-1 and its potential diagnostic and prognostic value in pulmonary diseases.Chinese medical journal pulmonary and critical care medicine · 2023Article
- Matrix Metalloproteinases in Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2023Review
- A2M Serves as Promising Biomarker for Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023Article
- Activation of angiotensin II type-2 receptor protects against cigarette smoke-induced COPD.Pharmacological research · 2020Article
- Leonurus sibiricus root extracts decrease airway remodeling markers expression in fibroblasts.Clinical and experimental immunology · 2020Article
- Alpha-1 Antitrypsin Deficiency: Have We Got the Right Proteinase?Chronic obstructive pulmonary diseases (Miami, Fla.) · 2020Review
- Integrated transcriptomic correlation network analysis identifies COPD molecular determinants.Scientific reports · 2020Article
- Increased nasal matrix metalloproteinase-1 and -9 expression in smokers with chronic rhinosinusitis and asthma.Scientific reports · 2019Article
- Increased Ratio of Matrix Metalloproteinase-9 (MMP-9)/Tissue Inhibitor Metalloproteinase-1 from Alveolar Macrophages in Chronic Asthma with a Fast Decline in FEVJournal of clinical medicine · 2019Article
- Impact of Matrix Metalloproteinase 9 on COPD Development in Polish Patients: Genetic Polymorphism, Protein Level, and Their Relationship with Lung Function.BioMed research international · 2018Article
- Protective Effects of Anti-IL17 on Acute Lung Injury Induced by LPS in Mice.Frontiers in pharmacology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAirway hyperresponsiveness (AHR) is associated with airway inflammation and a rapid decline in lung function and is a predictor of future risk of COPD among smokers. Alveolar macrophages (AMs) from patients with COPD release a greater amount of matrix metalloproteinase (MMP)-9. We hypothesized that the imbalance between MMP-9 and tissue inhibitor of metalloproteinase-1 (TIMP-1) is related to AHR in smokers. PATIENTS AND
methodsHealthy smokers with AHR (AHR + S) or smokers without AHR (AHR - S; divided according to a methacholine challenge test) and nonsmokers without AHR (AHR - NS) were enrolled. Spirometry was performed during enrollment and repeated after 5 years. Initially, AMs recovered from bronchoalveolar lavage (BAL) fluid were cultured in the presence of p38 mitogen-activated protein kinase (MAPK) inhibitor (SB203580), MAPK kinase (MEK) 1/2 (the MEK of extracellular signal-regulated kinase [ERK] inhibitor, PD98059), or medium alone for 24 h. The release of MMP-9 and TIMP-1 in culture supernatants was measured by enzyme-linked immunosorbent assay.
resultsA greater reduction in forced expiratory volume in 1 s (FEV
conclusionAMs of AHR + NS produce excessive MMP-9 over TIMP-1, which may be a predictor of the development of airway obstruction. Inhibition of p38 MAPK and ERK suppresses the generation of MMP-9 by AMs from smokers.
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