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Advance in Pathogenesis, Diagnosis, and Treatment of Chronic Obstructive Pulmonary Disease (COPD)

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: closed (15 September 2023) | Viewed by 12849

Special Issue Editors

Dr. Amanda Iglesias

E-Mail
Guest Editor
1. Instituto de Investigación Sanitaria Illes Balears (IdISBa), 07120 Palma de Mallorca, Spain
2. Centro de Investigación Biomédica en Red in Respiratory Diseases (CIBERES), 28029 Madrid, Spain
Interests: COPD; miRNAs; biomarker
Special Issues, Collections and Topics in MDPI journals
Dr. Kazufumi Nakamura

E-Mail Website
Guest Editor
Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Kita-ku, Okayama 700-8558, Japan
Interests: fish oil; postprandial hyperlipidemia; antioxidants; heart failure; hyperlipidemia; atherosclerosis; cardiomyopathy; pulmonary hypertension
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This special issue aims to summarize new advances in the treatment and diagnosis of COPD with a special focus on cutting-edged diagnostic/prognosis tools, potential treatments and novel pathogenic pathways involved in disease. Advances in understanding the natural history of COPD and the development of strategies to assess COPD early in the disease is crucial to lower disease mortality. In this context, different approaches, from basic to translational research would constitute a particularly relevant opportunity to join efforts in improving our knowledge on these topics. For this reason, we invite you to submit research articles, either through original research or review formats. We especially welcome manuscripts that focus on the early diagnosis of COPD.

Dr. Amanda Iglesias
Dr. Kazufumi Nakamura
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • early COPD
  • diagnosis
  • biomarker
  • pathogenic pathways
  • new treatments

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Published Papers (4 papers)

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Research

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11 pages, 3210 KiB  
Article
Attenuation of LPS-Induced Lung Injury by Benziodarone via Reactive Oxygen Species Reduction
by Tsutomu Ishihara, Ken-ichiro Tanaka, Ayaka Takafuji, Keita Miura and Tohru Mizushima
Int. J. Mol. Sci. 2023, 24(12), 10035; https://doi.org/10.3390/ijms241210035 - 12 Jun 2023
Cited by 1 | Viewed by 1546
Abstract
As overproduction of reactive oxygen species (ROS) causes various diseases, antioxidants that scavenge ROS, or inhibitors that suppress excessive ROS generation, can be used as therapeutic agents. From a library of approved drugs, we screened compounds that reduced superoxide anions produced by pyocyanin-stimulated [...] Read more.
As overproduction of reactive oxygen species (ROS) causes various diseases, antioxidants that scavenge ROS, or inhibitors that suppress excessive ROS generation, can be used as therapeutic agents. From a library of approved drugs, we screened compounds that reduced superoxide anions produced by pyocyanin-stimulated leukemia cells and identified benzbromarone. Further investigation of several of its analogues showed that benziodarone possessed the highest activity in reducing superoxide anions without causing cytotoxicity. In contrast, in a cell-free assay, benziodarone induced only a minimal decrease in superoxide anion levels generated by xanthine oxidase. These results suggest that benziodarone is an inhibitor of NADPH oxidases in the plasma membrane but is not a superoxide anion scavenger. We investigated the preventive effect of benziodarone on lipopolysaccharide (LPS)-induced murine lung injury as a model of acute respiratory distress syndrome (ARDS). Intratracheal administration of benziodarone attenuated tissue damage and inflammation via its ROS-reducing activity. These results indicate the potential application of benziodarone as a therapeutic agent against diseases caused by ROS overproduction. Full article
(This article belongs to the Special Issue Advance in Pathogenesis, Diagnosis, and Treatment of Chronic Obstructive Pulmonary Disease (COPD))
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15 pages, 1542 KiB  
Article
Mesenchymal Stem Cells from COPD Patients Are Capable of Restoring Elastase-Induced Emphysema in a Murine Experimental Model
by Carlos Río, Andreas K. Jahn, Aina Martin-Medina, Alba Marina Calvo Bota, Mª Teresa De Francisco Casado, Pere Joan Pont Antona, Orlando Gigirey Castro, Ángel Francisco Carvajal, Cristina Villena Portella, Cristina Gómez Bellvert, Amanda Iglesias, Javier Calvo Benito, Antoni Gayà Puig, Luis A. Ortiz and Ernest Sala-Llinàs
Int. J. Mol. Sci. 2023, 24(6), 5813; https://doi.org/10.3390/ijms24065813 - 18 Mar 2023
Cited by 3 | Viewed by 2553
Abstract
COPD is a chronic lung disease that affects millions of people, declining their lung function and impairing their life quality. Despite years of research and drug approvals, we are still not capable of halting progression or restoring normal lung function. Mesenchymal stem cells [...] Read more.
COPD is a chronic lung disease that affects millions of people, declining their lung function and impairing their life quality. Despite years of research and drug approvals, we are still not capable of halting progression or restoring normal lung function. Mesenchymal stem cells (MSC) are cells with extraordinary repair capacity, and MSC-based therapy brings future hope for COPD treatment, although the best source and route of administration are unclear. MSC from adipose tissue (AD-MSC) represents an option for autologous treatment; however, they could be less effective than donor MSC. We compared in vitro behavior of AD-MSC from COPD and non-COPD individuals by migration/proliferation assay, and tested their therapeutic potential in an elastase mouse model. In addition, we tested intravenous versus intratracheal routes, inoculating umbilical cord (UC) MSC and analyzed molecular changes by protein array. Although COPD AD-MSC have impaired migratory response to VEGF and cigarette smoke, they were as efficient as non-COPD in reducing elastase-induced lung emphysema. UC-MSC reduced lung emphysema regardless of the administration route and modified the inflammatory profile in elastase-treated mice. Our data demonstrate equal therapeutic potential of AD-MSC from COPD and non-COPD subjects in the pre-clinical model, thus supporting their autologous use in disease. Full article
(This article belongs to the Special Issue Advance in Pathogenesis, Diagnosis, and Treatment of Chronic Obstructive Pulmonary Disease (COPD))
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Review

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15 pages, 4876 KiB  
Review
The Role of IL-33/ST2 in COPD and Its Future as an Antibody Therapy
by Lluc Riera-Martínez, Laura Cànaves-Gómez, Amanda Iglesias, Aina Martin-Medina and Borja G. Cosío
Int. J. Mol. Sci. 2023, 24(10), 8702; https://doi.org/10.3390/ijms24108702 - 12 May 2023
Cited by 11 | Viewed by 4383
Abstract
COPD is a leading cause of mortality and morbidity worldwide and is associated with a high socioeconomic burden. Current treatment includes the use of inhaled corticosteroids and bronchodilators, which can help to improve symptoms and reduce exacerbations; however, there is no solution for [...] Read more.
COPD is a leading cause of mortality and morbidity worldwide and is associated with a high socioeconomic burden. Current treatment includes the use of inhaled corticosteroids and bronchodilators, which can help to improve symptoms and reduce exacerbations; however, there is no solution for restoring lung function and the emphysema caused by loss of the alveolar tissue. Moreover, exacerbations accelerate progression and challenge even more the management of COPD. Mechanisms of inflammation in COPD have been investigated over the past years, thus opening new avenues to develop novel targeted-directed therapies. Special attention has been paid to IL-33 and its receptor ST2, as they have been found to mediate immune responses and alveolar damage, and their expression is upregulated in COPD patients, which correlates with disease progression. Here we summarize the current knowledge on the IL-33/ST2 pathway and its involvement in COPD, with a special focus on developed antibodies and the ongoing clinical trials using anti-IL-33 and anti-ST2 strategies in COPD patients. Full article
(This article belongs to the Special Issue Advance in Pathogenesis, Diagnosis, and Treatment of Chronic Obstructive Pulmonary Disease (COPD))
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16 pages, 1178 KiB  
Review
Applying Next-Generation Sequencing and Multi-Omics in Chronic Obstructive Pulmonary Disease
by Pei Yee Tiew, Oliver W. Meldrum and Sanjay H. Chotirmall
Int. J. Mol. Sci. 2023, 24(3), 2955; https://doi.org/10.3390/ijms24032955 - 3 Feb 2023
Cited by 7 | Viewed by 3433
Abstract
Microbiomics have significantly advanced over the last decade, driven by the widespread availability of next-generation sequencing (NGS) and multi-omic technologies. Integration of NGS and multi-omic datasets allow for a holistic assessment of endophenotypes across a range of chronic respiratory disease states, including chronic [...] Read more.
Microbiomics have significantly advanced over the last decade, driven by the widespread availability of next-generation sequencing (NGS) and multi-omic technologies. Integration of NGS and multi-omic datasets allow for a holistic assessment of endophenotypes across a range of chronic respiratory disease states, including chronic obstructive pulmonary disease (COPD). Valuable insight has been attained into the nature, function, and significance of microbial communities in disease onset, progression, prognosis, and response to treatment in COPD. Moving beyond single-biome assessment, there now exists a growing literature on functional assessment and host–microbe interaction and, in particular, their contribution to disease progression, severity, and outcome. Identifying specific microbes and/or metabolic signatures associated with COPD can open novel avenues for therapeutic intervention and prognosis-related biomarkers. Despite the promise and potential of these approaches, the large amount of data generated by such technologies can be challenging to analyze and interpret, and currently, there remains a lack of standardized methods to address this. This review outlines the current use and proposes future avenues for the application of NGS and multi-omic technologies in the endophenotyping, prognostication, and treatment of COPD. Full article
(This article belongs to the Special Issue Advance in Pathogenesis, Diagnosis, and Treatment of Chronic Obstructive Pulmonary Disease (COPD))
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