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Chronic Obstructive Pulmonary Disease (COPD): Molecular Mechanisms and Treatment
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Chronic Obstructive Pulmonary Disease (COPD): Molecular Mechanisms and Treatment

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 (20 July 2024) | Viewed by 2623

Special Issue Editor

Dr. Ramcés Falfán-Valencia

E-Mail Website
Guest Editor
Sección XVI Tlalpan, Instituto Nacional de Enfermedades Respiratorias Ismael Cosio Villegas, Mexico City, Mexico
Interests: respiratory medicine; genetic epidemiology; immunology; human biology; genetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is supervised by Dr. Ramcés Falfán-Valencia and assisted by our Topical Advisory Panel members, Dr. Gloria Pérez-Rubio and Dr. Ingrid Fricke-Galindo.

We are pleased to invite you to contribute to our Special Issue of the International Journal of Molecular Sciences (IJMS), titled “Chronic Obstructive Pulmonary Disease (COPD): Molecular Mechanisms and Treatment”. This issue will cover a selection of recent research topics and current review articles, reporting the latest updates on COPD with a particular emphasis on physiopathological mechanisms and novel therapy approaches.

Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. COPD is a heterogeneous condition; the onset and trajectory are influenced by tobacco smoking, individual genetics, and the environmental exposures individuals accumulate over their life course. There is an urgent need to identify COPD patients at high risk for poor outcomes and understand mechanistically why some individuals are at high risk.

This issue can be addressed by precision medicine approaches, which focus on understanding an individual’s disease risk and tailoring management based on pathobiology, environmental exposures, and biomarkers. Genetics, omics, and network analytic techniques have started to dissect COPD heterogeneity and identify patients with specific pathobiology. Phenotyping individuals based on similar clinical or molecular characteristics can guide appropriate therapeutic management. Treatable traits, characteristics for which evidence supports a treatment response, are being increasingly incorporated into COPD clinical guidelines. However, the COPD phenotyping literature is changing. Innovations in lung imaging, physiologic metrics, omics, and biomarker technologies contribute to a better understanding of COPD heterogeneity.

Dr. Ramcés Falfán-Valencia
Guest Editor

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

  • emphysema
  • chronic bronchitis
  • genetic susceptibility
  • pharmacogenomics
  • exacerbation
  • biomarkers
  • inflammasome
  • genomics
  • nicotine addiction and COPD
  • biomass-burning smoke

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Published Papers (2 papers)

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Research

10 pages, 1617 KiB  
Article
Loss of JCAD/KIAA1462 Protects the Lung from Acute and Chronic Consequences of Chronic Obstructive Pulmonary Disease
by Ratoe Suraya, Tatsuya Nagano, Masako Yumura, Tetsuya Hara, Masaya Akashi, Masatsugu Yamamoto, Motoko Tachihara, Yoshihiro Nishimura and Kazuyuki Kobayashi
Int. J. Mol. Sci. 2024, 25(17), 9492; https://doi.org/10.3390/ijms25179492 - 31 Aug 2024
Viewed by 725
Abstract
Even with recent advances in pathobiology and treatment options, chronic obstructive pulmonary disease (COPD) remains a major contributor to morbidity and mortality. To develop new ways of combating this disease, breakthroughs in our understanding of its mechanisms are sorely needed. Investigating the involvement [...] Read more.
Even with recent advances in pathobiology and treatment options, chronic obstructive pulmonary disease (COPD) remains a major contributor to morbidity and mortality. To develop new ways of combating this disease, breakthroughs in our understanding of its mechanisms are sorely needed. Investigating the involvement of underanalyzed lung cell types, such as endothelial cells (ECs), is one way to further our understanding of COPD. JCAD is a junctional protein in endothelial cells (ECs) arising from the KIAA1462 gene, and a mutation in this gene has been implicated in the risk of developing COPD. In our study, we induced inflammation and emphysema in mice via the global knockout of KIAA1462/JCAD (JCAD-KO) and confirmed it in HPMECs and A549 to examine how the loss of JCAD could affect COPD development. We found that KIAA1462/JCAD loss reduced acute lung inflammation after elastase treatment. Even after 3 weeks of elastase, JCAD-KO mice demonstrated a preserved lung parenchymal structure and vasculature. In vitro, after KIAA1462 expression is silenced, both endothelial and epithelial cells showed alterations in pro-inflammatory gene expression after TNF-α treatment. We concluded that JCAD loss could ameliorate COPD through its anti-inflammatory and anti-angiogenic effects, and that KIAA1462/JCAD could be a novel target for COPD therapy. Full article
(This article belongs to the Special Issue Chronic Obstructive Pulmonary Disease (COPD): Molecular Mechanisms and Treatment)
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17 pages, 3600 KiB  
Article
Role of the Fungus Pneumocystis in IL1β Pathway Activation and Airways Collagen Deposition in Elastase-Induced COPD Animals
by Krishna Coronado, Carla Herrada and Diego A. Rojas
Int. J. Mol. Sci. 2024, 25(6), 3150; https://doi.org/10.3390/ijms25063150 - 9 Mar 2024
Viewed by 1355
Abstract
Inflammation and mucus production are prevalent characteristics of chronic respiratory conditions, such as asthma and chronic chronic obstructive pulmonary disease (COPD). Biological co-factors, including bacteria, viruses, and fungi, may exacerbate these diseases by activating various pathways associated with airway diseases. An example is [...] Read more.
Inflammation and mucus production are prevalent characteristics of chronic respiratory conditions, such as asthma and chronic chronic obstructive pulmonary disease (COPD). Biological co-factors, including bacteria, viruses, and fungi, may exacerbate these diseases by activating various pathways associated with airway diseases. An example is the fungus Pneumocystis, which is linked to severe COPD in human patients. Recent evidence has demonstrated that Pneumocystis significantly enhanced inflammation and mucus hypersecretion in a rat model of elastase-induced COPD. The present study specifically aims to investigate two additional aspects associated with the pathology induced by Pneumocystis infection: inflammation and collagen deposition around airways. To this end, the focus was to investigate the role of the IL-1β pro-inflammatory pathway during Pneumocystis infection in COPD rats. Several airway pathology-related features, such as inflammation, mucus hypersecretion, and fibrosis, were evaluated using histological and molecular techniques. COPD animals infected with Pneumocystis exhibited elevated inflammation levels, including a synergistic increase in IL-1β and Cox-2. Furthermore, protein levels of the IL-1β-dependent transcription factor cAMP response element-binding (CREB) showed a synergistic elevation of their phosphorylated version in the lungs of COPD animals infected with Pneumocystis, while mucus levels were notably higher in the airways of COPD-infected animals. Interestingly, a CREB responsive element (CRE) was identified in the Muc5b promoter. The presence of CREB in the Muc5b promoter was synergistically increased in COPD animals infected with Pneumocystis compared to other experimental groups. Finally, an increment of deposited collagen was identified surrounding the airways of COPD animals infected with Pneumocystis compared with the other experimental animal groups and correlated with the increase of Tgfβ1 mRNA levels. These findings emphasize the role of Pneumocystis as a potential biological co-factor in chronic respiratory diseases like COPD or asthma, warranting new perspectives in the treatment of chronic respiratory diseases. Full article
(This article belongs to the Special Issue Chronic Obstructive Pulmonary Disease (COPD): Molecular Mechanisms and Treatment)
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