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Molecular Mechanisms and Therapies of Chronic Obstructive Pulmonary Disease
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Molecular Mechanisms and Therapies of Chronic Obstructive Pulmonary Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 July 2025 | Viewed by 11627

Special Issue Editor

Dr. Marija Stankovic

E-Mail Website
Guest Editor
Laboratory for Molecular Biology, Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, 11042 Belgrade, Serbia
Interests: chronic lung disorders; COPD; bronchiectasis; emphysema and fibrosis; inflammation; oxidative stress; metabolism of xenobiotics; remodeling of extracellular matrix; genetic and molecular mechanisms

Special Issue Information

Dear Colleagues,

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide, representing a serious concern for the healthcare system and significant socioeconomic burden. The pathogenesis of COPD is complex, characterized by persistent inflammation of the lungs caused by noxious particles or gases such as cigarette smoke and air pollutants. Lung inflammation increases with the progress of disease, and it is amplified during acute exacerbations which are associated with significant morbidity and mortality. Despite tremendous efforts in the development of research on this topic, the mechanisms of the etiopathogenesis of COPD are not completely understood, which precludes the existence of curative pharmacological treatment.

Nevertheless, the main anti-inflammatory therapy for COPD includes corticosteroids, which are not necessarily efficient in the suppression of lung inflammation, cannot restore impaired and lost lung tissue and decline in lung function, and have severe adverse effects. Therefore, there is an urgent need to develop a novel, safe and effective therapy that will eliminate the symptoms of the disease and stimulate the repair of damaged lung tissue. As a heterogenous condition, COPD may also require the application of personalized medicine.

Recently, novel molecular mechanisms of the pathogenesis of COPD have been recognized, which opens up possibilities for the development of targeted therapies. COPD represents an opportunity for research on numerous aspects, which potentiates the finding of an adequate pharmacological intervention. This Special Issue invites authors to submit original research articles and review articles that summarize current advances in research, diagnostic, prevention, and therapy of COPD. The aim of this Special Issue is to provide an open access to novel data and clues about the molecular basis of COPD so that we can ultimately progress our capabilities in the creation of a curable treatment for this common chronic lung disease.

Dr. Marija Stanković
Guest Editor

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Keywords

  • COPD
  • molecular mechanism
  • inflammation
  • therapy

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Published Papers (5 papers)

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Research

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15 pages, 2285 KiB  
Article
Impaired SERPIN–Protease Balance in the Peripheral Lungs of Stable COPD Patients
by Antonino Di Stefano, Francesco Nucera, Umberto Rosani, Paola Brun, Isabella Gnemmi, Mauro Maniscalco, Silvestro Ennio D’Anna, Andrea Leonardi, Vitina Carriero, Francesca Bertolini, Josè Freni, Antonio Ieni, Sebastiano Gangemi, Paolo Ruggeri and Fabio Luigi Massimo Ricciardolo
Int. J. Mol. Sci. 2025, 26(7), 2832; https://doi.org/10.3390/ijms26072832 - 21 Mar 2025
Viewed by 293
Abstract
The protease–antiprotease balance is involved in many biological processes, including blood coagulation, tissue remodeling, inflammation and immune responses. The aim of this study is to determine the balance between SERPINs and some related proteases in the lungs of stable COPD patients. In this [...] Read more.
The protease–antiprotease balance is involved in many biological processes, including blood coagulation, tissue remodeling, inflammation and immune responses. The aim of this study is to determine the balance between SERPINs and some related proteases in the lungs of stable COPD patients. In this cross-sectional study, the expression and localization of human SERPINs (anti-proteases) and some related proteases were measured in the lung parenchyma of mild-moderate COPD (MCOPD, n = 13) patients, control smokers (CS, n = 14) and control nonsmokers (CNS, n = 12) using transcriptome analysis, immunohistochemistry, and ELISA tests. Peripheral lung transcriptomic data showed increased mRNA levels of tissue plasminogen activator (tPA), cathepsin-L and caspase-1 as well as increased SERPINs A6, B3, B5, B11, B13 in the COPD group compared to the CNS group. At the protein level, IHC analysis showed that tPA and cathepsin-L increased in the bronchiolar epithelium and alveolar septa of the CS and COPD groups compared to the CNS group, as well as SERPINB5 and B13 in the alveolar macrophages and alveolar septa of the CS and COPD groups compared to the CNS group. SERPINA6 was shown to be decreased in the bronchiolar epithelium, bronchiolar lamina propria, and alveolar septa of the CS and COPD groups compared to the CNS group and was positively correlated with lung function. SERPINB3 was decreased in the alveolar septa of the CS group compared to the CNS group. The ELISA tests showed that in the total lung extracts, decreased levels of SERPINA6 and increased caspase-1 were shown in the COPD group compared to the CNS or both control groups, respectively. These data show an imbalance, at the protein level, of SERPINs and some related proteases in the lungs of the CS and stable COPD groups. These alterations may play a role in damaging the lung parenchyma of susceptible COPD patients. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapies of Chronic Obstructive Pulmonary Disease)
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16 pages, 3763 KiB  
Article
Expression of Stress-Induced Genes in Bronchoalveolar Lavage Cells and Lung Fibroblasts from Healthy and COPD Subjects
by Martin Garcia-Ryde, Nicole M. D. van der Burg, Frida Berlin, Gunilla Westergren-Thorsson, Leif Bjermer, Jaro Ankerst, Anna-Karin Larsson-Callerfelt, Cecilia K. Andersson and Ellen Tufvesson
Int. J. Mol. Sci. 2024, 25(12), 6600; https://doi.org/10.3390/ijms25126600 - 15 Jun 2024
Cited by 1 | Viewed by 1155
Abstract
Chronic obstructive pulmonary disease (COPD) is commonly caused from smoking cigarettes that induce biological stress responses. Previously we found disorganized endoplasmic reticulum (ER) in fibroblasts from COPD with different responses to chemical stressors compared to healthy subjects. Here, we aimed to investigate differences [...] Read more.
Chronic obstructive pulmonary disease (COPD) is commonly caused from smoking cigarettes that induce biological stress responses. Previously we found disorganized endoplasmic reticulum (ER) in fibroblasts from COPD with different responses to chemical stressors compared to healthy subjects. Here, we aimed to investigate differences in stress-related gene expressions within lung cells from COPD and healthy subjects. Bronchoalveolar lavage (BAL) cells were collected from seven COPD and 35 healthy subjects. Lung fibroblasts were derived from 19 COPD and 24 healthy subjects and exposed to cigarette smoke extract (CSE). Gene and protein expression and cell proliferation were investigated. Compared to healthy subjects, we found lower gene expression of CHOP in lung fibroblasts from COPD subjects. Exposure to CSE caused inhibition of lung fibroblast proliferation in both groups, though the changes in ER stress-related gene expressions (ATF6, IRE1, PERK, ATF4, CHOP, BCL2L1) and genes relating to proteasomal subunits mostly occurred in healthy lung fibroblasts. No differences were found in BAL cells. In this study, we have found that lung fibroblasts from COPD subjects have an atypical ER stress gene response to CSE, particularly in genes related to apoptosis. This difference in response to CSE may be a contributing factor to COPD progression. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapies of Chronic Obstructive Pulmonary Disease)
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Review

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14 pages, 684 KiB  
Review
Molecular Approaches to Treating Chronic Obstructive Pulmonary Disease: Current Perspectives and Future Directions
by Sheryl-Phuc Vu, Kaleb Veit and Ruxana T. Sadikot
Int. J. Mol. Sci. 2025, 26(5), 2184; https://doi.org/10.3390/ijms26052184 - 28 Feb 2025
Viewed by 966
Abstract
Chronic obstructive pulmonary disease (COPD) is a clinical syndrome that presents as airflow limitation with poor reversibility accompanied by dynamic hyperinflation of the lung. It is a complex disease with chronic inflammatory airway changes caused by exposure to noxious particles or gases, such [...] Read more.
Chronic obstructive pulmonary disease (COPD) is a clinical syndrome that presents as airflow limitation with poor reversibility accompanied by dynamic hyperinflation of the lung. It is a complex disease with chronic inflammatory airway changes caused by exposure to noxious particles or gases, such as cigarette smoke. The disease involves persistent inflammation and oxidative stress, perpetuated by frequent exacerbations. The prevalence of COPD is on the rise, with the prediction that it will be the leading cause of morbidity and mortality over the next decade. Despite the global burden of COPD and its associated morbidity and mortality, treatment remains limited. Although the understanding of the pathogenesis of COPD has increased over the last two decades, molecular approaches to develop new therapies for the treatment of COPD have lagged. Here, we review the molecular approaches that have the potential for developing novel therapies for COPD. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapies of Chronic Obstructive Pulmonary Disease)
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23 pages, 662 KiB  
Review
Lung Microbiota: From Healthy Lungs to Development of Chronic Obstructive Pulmonary Disease
by Marija M. Stankovic
Int. J. Mol. Sci. 2025, 26(4), 1403; https://doi.org/10.3390/ijms26041403 - 7 Feb 2025
Cited by 1 | Viewed by 1238
Abstract
Lung health is dependent on a complex picture of the lung microbiota composed of bacteriobiota, mycobiota, and virome. The studies have demonstrated that the lung microbiota has a crucial role in host protection by regulating innate and adaptive lung immunity. Chronic obstructive pulmonary [...] Read more.
Lung health is dependent on a complex picture of the lung microbiota composed of bacteriobiota, mycobiota, and virome. The studies have demonstrated that the lung microbiota has a crucial role in host protection by regulating innate and adaptive lung immunity. Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease featuring changed microbiota composition and diversity, known as a dysbiosis. The lung dysbiosis increases with the progress of COPD and during exacerbation. Two models of dysbiosis have been proposed: dysbiosis and inflammation cycles and the disturbance of bacterial interactome. Still, it is unknown if the driving factor of the pathogenesis of COPD belongs to the host or microbiota. Recently, host–microbiota and microbe–microbe interactions have been highlighted in COPD, but the mechanisms behind these interactions need further exploration. The function of the gut–lung axis is crucial for the maintenance of lung health and is affected in COPD. The application of probiotics has resulted in host–beneficial effects, and it is likely that future progress in this field will aid in the therapy of COPD. In this review, the composition of the lung microbiota, molecular mechanisms, and clinical aspects relating to host and microbiota in health and COPD are comprehensively provided. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapies of Chronic Obstructive Pulmonary Disease)
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14 pages, 657 KiB  
Review
Exploring Molecular Mechanisms and Biomarkers in COPD: An Overview of Current Advancements and Perspectives
by Chin-Ling Li and Shih-Feng Liu
Int. J. Mol. Sci. 2024, 25(13), 7347; https://doi.org/10.3390/ijms25137347 - 4 Jul 2024
Cited by 12 | Viewed by 6247
Abstract
Chronic obstructive pulmonary disease (COPD) plays a significant role in global morbidity and mortality rates, typified by progressive airflow restriction and lingering respiratory symptoms. Recent explorations in molecular biology have illuminated the complex mechanisms underpinning COPD pathogenesis, providing critical insights into disease progression, [...] Read more.
Chronic obstructive pulmonary disease (COPD) plays a significant role in global morbidity and mortality rates, typified by progressive airflow restriction and lingering respiratory symptoms. Recent explorations in molecular biology have illuminated the complex mechanisms underpinning COPD pathogenesis, providing critical insights into disease progression, exacerbations, and potential therapeutic interventions. This review delivers a thorough examination of the latest progress in molecular research related to COPD, involving fundamental molecular pathways, biomarkers, therapeutic targets, and cutting-edge technologies. Key areas of focus include the roles of inflammation, oxidative stress, and protease–antiprotease imbalances, alongside genetic and epigenetic factors contributing to COPD susceptibility and heterogeneity. Additionally, advancements in omics technologies—such as genomics, transcriptomics, proteomics, and metabolomics—offer new avenues for comprehensive molecular profiling, aiding in the discovery of novel biomarkers and therapeutic targets. Comprehending the molecular foundation of COPD carries substantial potential for the creation of tailored treatment strategies and the enhancement of patient outcomes. By integrating molecular insights into clinical practice, there is a promising pathway towards personalized medicine approaches that can improve the diagnosis, treatment, and overall management of COPD, ultimately reducing its global burden. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapies of Chronic Obstructive Pulmonary Disease)
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