Pathogenesis, Diagnosis, and Treatment of Respiratory Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 4352

Special Issue Editor


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Guest Editor
1. School of Medicine, China Medical University, Taichung, Taiwan
2. Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan
Interests: COPD; asthma; interstitial lung disease; lung cancer; pneumonia; tuberculosis; respiratory failure; ARDS; COVID-19; obstructive sleep apnea
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Special Issue Information

Dear Colleagues,

COVID-19 has had a huge impact on our lives. Thus, we must pay more attention to respiratory diseases, particularly their molecular mechanisms, diagnosis, and treatment. These actions will directly affect and contribute to the survival of human beings.

This Special Issue aims to collect various research articles on respiratory diseases. Studies focusing on the molecular mechanisms, pathogenesis, diagnosis, treatment, and prognosis of these diseases will be prioritized. This Special Issue will improve our understanding of the occurrence of respiratory diseases and possible approaches to early diagnosis and precise treatment.

In this Special Issue, original clinical and basic research articles and reviews are welcome. Research areas may include (but are not limited to) the following: COPD, asthma, interstitial lung disease, lung cancer, pneumonia, tuberculosis, respiratory failure, ARDS, COVID-19, and obstructive sleep apnea. I look forward to receiving your contributions.

Dr. Te-Chun Shen
Guest Editor

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Keywords

  • COPD
  • asthma
  • interstitial lung disease
  • lung cancer
  • pneumonia
  • tuberculosis
  • respiratory failure
  • ARDS
  • COVID-19
  • obstructive sleep apnea

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Published Papers (3 papers)

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Research

10 pages, 237 KB  
Article
Exploring the Associations Between CHRNA5 and IREB2 Gene Polymorphisms and COPD in the Kazakhstan Population
by Almira Akparova, Gaukhar Kurmanova, Gulzhan Trimova, Yeldar Ashirbekov, Diana Nigmatova, Balkiya Abdrakhmanova, Zhanar Mussagulova, Gulzhana Idrisova, Anarkul Kulembayeva and Almagul Kurmanova
Biomedicines 2025, 13(9), 2260; https://doi.org/10.3390/biomedicines13092260 - 13 Sep 2025
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Abstract
Background/Objectives: Chronic obstructive pulmonary disease (COPD) is a progressive inflammatory lung disease characterized by irreversible airway obstruction. This study aims to investigate the associations between COPD and its phenotypes with polymorphic variants of the IREB2 and CHRNA5 genes in the Kazakhstan population. [...] Read more.
Background/Objectives: Chronic obstructive pulmonary disease (COPD) is a progressive inflammatory lung disease characterized by irreversible airway obstruction. This study aims to investigate the associations between COPD and its phenotypes with polymorphic variants of the IREB2 and CHRNA5 genes in the Kazakhstan population. Methods: A case–control study was conducted involving 265 COPD patients and 267 controls. Genotyping of the IREB2 polymorphisms rs13180 and rs2568494, as well as CHRNA5 rs16969968 polymorphism, was performed using real-time polymerase chain reactions (Real-Time PCRs). Results: A higher frequency of the AA genotype of the IREB2 rs2568494 polymorphism was identified in COPD patients with moderate to very severe airflow obstruction (Chronic Obstructive Lung Disease (GOLD) stages II, III, and IV), with an odds ratio of 0.69 (95% CI = 0.23–2.10; Padj = 0.03). The IREB2 rs13180 polymorphism was significantly more frequent or prevalent in smokers and showed a correlation with FEV1 (forced expiratory volume in one second) (β = 7.79, SE = 2.98, p = 0.01) and FEV1/ FVC (forced vital capacity) (β = 9.51, SE = 2.95, p = 0.002). Additionally, the CC genotype of this polymorphism was associated with clinical manifestations of COVID-19 in COPD patients (χ2= 3,95, df = 2, p = 0.05). Conclusions: Our study identified a significant association between the IREB2 rs2568494 polymorphism and an increased risk of severe COPD. The IREB2 rs13180 polymorphism was linked to smoking behavior, as well as key lung function indicators, suggesting its potential role in disease progression and lung damage. Furthermore, the CC genotype of the IREB2 rs13180 polymorphism was associated with clinical manifestations of COVID-19 in COPD patients, indicating a potential impact of this genetic variant on susceptibility to viral infections in this population. Full article
(This article belongs to the Special Issue Pathogenesis, Diagnosis, and Treatment of Respiratory Diseases)
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12 pages, 1014 KB  
Article
Immunohistochemical Analysis of Mastocyte Inflammation: A Comparative Study of COPD Associated with Tobacco Smoking and Wood Smoke Exposure
by Robinson Robles-Hernández, Rosa María Rivera, Marcos Páramo-Pérez, Dulce Mariana Quiroz-Camacho, Gustavo I. Centeno-Saenz, Alan Bedolla-Tinoco, María C. Maya-García and Rogelio Pérez-Padilla
Biomedicines 2025, 13(7), 1593; https://doi.org/10.3390/biomedicines13071593 - 30 Jun 2025
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Abstract
Background: Chronic Obstructive Pulmonary Disease (COPD) exhibits some phenotypic differences between patients with biomass smoke inhalation (COPD-B) and tobacco smoking (COPD-T). COPD-B is characterized by less emphysema but more airway disease and vascular pulmonary remodeling, which are related to mast cells in lung [...] Read more.
Background: Chronic Obstructive Pulmonary Disease (COPD) exhibits some phenotypic differences between patients with biomass smoke inhalation (COPD-B) and tobacco smoking (COPD-T). COPD-B is characterized by less emphysema but more airway disease and vascular pulmonary remodeling, which are related to mast cells in lung tissues in COPD-T. Our objective was to describe the differences between the number of mast cells in COPD-B and COPD-T patients. Methods: A cross-sectional study was conducted on lung tissue resections for suspected cancer obtained between 2014 and 2021 from patients with documented COPD due to wood smoke or tobacco exposure. Histological samples were analyzed for mast cell count, CD34+ expression, and structural changes in lung tissue and pulmonary circulation. Results: A total of 20 histological samples were analyzed, with significant differences found in mast cell count [median 8 (p25-75, 5–11) vs. 2 (p75-25, 0–6), p = 0.016] and severe peribronchiolar fibrosis (60% vs. 10%, p = 0.04) between COPD-B and COPD-T patients. A positive correlation [Spearman rho = 0.879 (95% CI 0.71–0.96), p < 0.001] was observed between mast cell count and a gradual increase in pulmonary artery diameter. Conclusions: These preliminary findings suggest histological differences and the presence of mast cells between COPD-B and COPD-T, which should be confirmed in a larger number of samples and patients. Full article
(This article belongs to the Special Issue Pathogenesis, Diagnosis, and Treatment of Respiratory Diseases)
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15 pages, 5770 KB  
Article
PGC1-Alpha/Sirt3 Signaling Pathway Mediates the Anti-Pulmonary Fibrosis Effect of Hirudin by Inhibiting Fibroblast Senescence
by Bin He, Qian Zeng, Yumei Tian, Yuyang Luo, Minlin Liao, Wenjie Huang, Bin Wu, Ziqiang Luo, Xiaoting Huang, Wei Liu and Siyuan Tang
Biomedicines 2024, 12(7), 1436; https://doi.org/10.3390/biomedicines12071436 - 27 Jun 2024
Cited by 4 | Viewed by 2285
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive fibrotic lung disease for which there is a lack of effective pharmacological treatments. Hirudin, a natural peptide extracted from leeches, has been used for broad pharmacological purposes. In this study, we investigated the therapeutic effects [...] Read more.
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive fibrotic lung disease for which there is a lack of effective pharmacological treatments. Hirudin, a natural peptide extracted from leeches, has been used for broad pharmacological purposes. In this study, we investigated the therapeutic effects of hirudin on IPF and its related mechanism of action. By constructing a mouse model of pulmonary fibrosis and treating it with hirudin in vivo, we found that hirudin exerted anti-fibrotic, anti-oxidative, and anti-fibroblast senescence effects. Moreover, using an in vitro model of stress-induced premature senescence in primary mouse lung fibroblasts and treating with hirudin, we observed inhibition of fibroblast senescence and upregulation of PGC1-alpha and Sirt3 expression. However, specific silencing of PGC1-alpha or Sirt3 suppressed the anti-fibroblast senescence effect of hirudin. Thus, the PGC1-alpha/Sirt3 pathway mediates the anti-fibroblast senescence effect of hirudin, potentially serving as a molecular mechanism underlying its anti-fibrosis and anti-oxidative stress effects exerted on the lungs. Full article
(This article belongs to the Special Issue Pathogenesis, Diagnosis, and Treatment of Respiratory Diseases)
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