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Cells
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Advances in COPD II
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Advances in COPD II

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (1 April 2023) | Viewed by 1179

Special Issue Editors

Dr. Davina C. M. Simoes

E-Mail Website
Guest Editor
Faculty of Health and Life Sciences, Northumbria University, Newcastle-upon-Tyne NE1 8ST, UK
Interests: COPD; asthma; muscle sarcopenia and cachexia; 3D-engineered muscle; extracellular matrix
Special Issues, Collections and Topics in MDPI journals
Dr. Esther Barreiro

E-Mail Website
Guest Editor
Pulmonology Department, Lung Cancer and Muscle Research Group, Hospital del Mar-IMIM, Parc de Salut Mar, Health and Experimental Sciences Department (CEXS), Universitat Pompeu Fabra (UPF), CIBERES, Barcelona, Spain
Interests: COPD
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chronic obstructive pulmonary disease (COPD) is the third world leading cause of death. COPD is a complex disease presenting airflow obstruction alongside systemic conditions associated with inflammation and alterations in repair mechanisms. Among the risk factors, the inhalation of cigarette smoke and other harmful particles is the most prominent. Synergistic effects such as excess body fat, poor nutrition, respiratory infections during childhood, and poor housing conditions are associated with a higher prevalence of COPD. Comorbid disease potentiates the morbidity of COPD, leading to hospitalizations, mortality, and healthcare costs. The complexity and heterogeneity of this disease hinder the development of novel treatments. New data on possible basic mechanisms at the cellular and molecular level addressing the complexity and heterogeneity of lung and systemic COPD will support advances in health treatment and care. 

This Special Issue aims to summarize advances in the COPD area of research, including studies on epidemiology, diagnostics tools, the basic mechanisms in COPD, pharmacotherapy, rehabilitation, and skeletal muscle comorbidity and emerging therapies. 

We look forward to your contribution

Dr. Davina C. M. Simoes
Dr. Esther Barreiro
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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • progress on COPD research
  • epidemiological insights
  • diagnostics tools
  • physiological insights
  • clinical management
  • non-pharmacological therapeutic strategies
  • new insights on pharmacological treatments

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Published Papers (1 paper)

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Research

8 pages, 817 KiB  
Article
IL13 Promoter (−1055) Polymorphism Associated with Leukocyte Mitochondria DNA Copy Number in Chronic Obstructive Pulmonary Disease
by Shih-Feng Liu, Hui-Chuan Chang, Yu-Ping Chang, Ho-Chang Kuo and Yuh-Chyn Tsai
Cells 2022, 11(23), 3787; https://doi.org/10.3390/cells11233787 - 26 Nov 2022
Cited by 2 | Viewed by 916
Abstract
IL13 polymorphism is associated with chronic obstructive pulmonary disease (COPD). Patients with COPD have smaller numbers of mitochondria deoxyribonucleic acid copies (mtDNA-CN) than people without COPD do. However, whether IL13 polymorphism affects the mutation and recombination of mitochondria remains unclear. Data for patients [...] Read more.
IL13 polymorphism is associated with chronic obstructive pulmonary disease (COPD). Patients with COPD have smaller numbers of mitochondria deoxyribonucleic acid copies (mtDNA-CN) than people without COPD do. However, whether IL13 polymorphism affects the mutation and recombination of mitochondria remains unclear. Data for patients with COPD and non-COPD were collected from Kaohsiung Chang Gung Memorial Hospital to enable a comparison of their leukocyte mtDNA-CN and the association of this information with IL-13 promoter (−1055) polymorphism. This study included 99 patients with COPD and 117 individuals without COPD. The non-COPD individuals included 77 healthy individuals that never smoked and 40 healthy smokers. The patients with COPD exhibited significantly lower mtDNA-CN than non-COPD did (250.34 vs. 440.03; p < 0.001); mtDNA-CN was particularly pronounced in individuals with the IL13 CC and CT genotypes compared with individuals with the TT genotype. When only individuals without COPD were considered and when all participants were considered, the differences in the mtDNA-CNs in individuals with the CC and CT genotypes were more significant than those in individuals with the TT genotype (448.4 and 533.6 vs. 282.8; p < 0.05 in non-COPD group); (368.8 and 362.6 vs. 249.6, p < 0.05 in all participants). The increase mtDNA-CN in the CC and CT genotypes was also more than that in the TT genotype in COPD patients, but showed no significance (260.1 and 230.5 vs. 149.9; p = 0.343). The finding shows that COPD is a mitochondria regulatory disorder and IL-13 promoter (−1055) polymorphism is associated with leukocyte mtDNA-CN. Developing COPD control methods based on mitochondrial regulation will be possible. Full article
(This article belongs to the Special Issue Advances in COPD II)
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