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Biomolecules
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Molecular Pathology, Diagnostics, and Therapeutics of Lung Disease
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Molecular Pathology, Diagnostics, and Therapeutics of Lung Disease

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 30 June 2026 | Viewed by 4965

Special Issue Editor

Dr. Toshimitsu Yamaoka

E-Mail Website
Guest Editor
Advanced Cancer Translational Research Institute, Showa University, Tokyo 142-8555, Japan
Interests: Ras mutations; Ras targeting inhibitor; resistance to Ras inhibition; potential combination therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Respiratory diseases are extremely diverse and include infectious diseases, bronchial asthma, chronic obstructive pulmonary disease, lung cancer, interstitial lung disease, and more. Each condition presents unique and complex challenges. In recent years, diagnosis and treatment in these areas have steadily evolved and are poised for continued development. By gathering studies to share and discuss latest findings in this Special Issue, we hope to spark a movement in research and development, leading to new diagnostic and treatment methods and bringing about major changes.

The keyword for this Special Issue is "exchange". For each field to evolve, the true nature of a disease must be identified. To uncover this, various ideas must be developed, and hypotheses must be formulated and proven. New trends can be created by engaging in this Special Issue. Hypothesis and proof are the essence of medical research. Let us gather, discuss, and consider the mystery of the respiratory system.

We believe that the results will not only contribute to the development of this Special Issue but will also contribute to appropriate medical treatment and the provision of safe and secure medical care.

We hope to make this Special Issue a success together with all of you. We look forward to your submissions.

Dr. Toshimitsu Yamaoka
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 250 words) can be sent to the Editorial Office for assessment.

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. Biomolecules is an international peer-reviewed open access monthly 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

  • pulmonary diseases
  • diagnostics
  • therapeutics

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Published Papers (4 papers)

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Research

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13 pages, 1032 KB  
Article
The Association Between the Eosinophilic COPD Phenotype with Overall Survival and Exacerbations in Patients on Long-Term Non-Invasive Ventilation
by Andras Bikov, Balazs Csoma, Andrew Chai, Eleonor Croft, Zsofia Lazar and Andrew Bentley
Biomolecules 2025, 15(12), 1728; https://doi.org/10.3390/biom15121728 - 12 Dec 2025
Viewed by 770
Abstract
Background: Long-term non-invasive ventilation (LT-NIV) can prolong life expectancy and may reduce the number of exacerbations in patients with COPD. The eosinophilic phenotype has recently gained significant attention as a treatable trait in COPD. However, it is less known how this phenotype relates [...] Read more.
Background: Long-term non-invasive ventilation (LT-NIV) can prolong life expectancy and may reduce the number of exacerbations in patients with COPD. The eosinophilic phenotype has recently gained significant attention as a treatable trait in COPD. However, it is less known how this phenotype relates to exacerbations and mortality in patients who are set up on LT-NIV. Methods: A total of 191 patients with COPD (65 ± 8 years, 55% women) who were setup on LT-NIV and followed-up (28/15–49/months) at our tertiary centre were analysed. The eosinophilic phenotype was defined by using an accepted cutoff for blood eosinophil count (≥300 cells/µL). Results: A total of 37 patients had the eosinophilic phenotype (66 ± 9 years, 60% women). There was a higher reduction in the number of exacerbations (1.0/−1.0–3.2/ vs. 0.05/−1.4–1.63/, p < 0.01) and a trend for a reduction in the rate of hospitalisations (1.0/−1.0–2.0/ vs. 0.0/0.0–1.0/, p = 0.07) post-NIV setup in the eosinophilic group. Most importantly, patients with high eosinophil counts had longer overall survival (34/15–74/ vs. 28/15–47/ months, p = 0.02, adjusted for covariates). Conclusions: The eosinophilic COPD phenotype seems to show better clinical responses to long-term NIV than patients without this trait. Further mechanistic studies are warranted to analyse this association. Full article
(This article belongs to the Special Issue Molecular Pathology, Diagnostics, and Therapeutics of Lung Disease)
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16 pages, 15295 KB  
Article
Small RNA Profiles of Serum-Derived Extracellular Vesicles in the Comorbid Condition of Frailty and Obstructive Pulmonary Disease: An Observational, Cross-Sectional Study
by Keiko Doi, Tsunahiko Hirano, Naoomi Tominaga, Kenji Watanabe, Keiji Oishi, Ayumi Fukatsu-Chikumoto, Tasuku Yamamoto, Yuichi Ohteru, Kazuki Hamada, Yoriyuki Murata, Maki Asami-Noyama, Nobutaka Edakuni, Tomoyuki Kakugawa, Yoichi Mizukami and Kazuto Matsunaga
Biomolecules 2025, 15(12), 1663; https://doi.org/10.3390/biom15121663 - 28 Nov 2025
Viewed by 598
Abstract
Frailty is increasingly recognized as a systemic complication in patients with obstructive pulmonary diseases (OPDs), yet its molecular basis remains unclear. Extracellular vesicles (EVs), which transport small RNAs, may offer mechanistic insight into this comorbidity. This study investigated the association between serum-derived EV [...] Read more.
Frailty is increasingly recognized as a systemic complication in patients with obstructive pulmonary diseases (OPDs), yet its molecular basis remains unclear. Extracellular vesicles (EVs), which transport small RNAs, may offer mechanistic insight into this comorbidity. This study investigated the association between serum-derived EV small RNAs and frailty in OPD. Sixty-eight patients with OPD were enrolled, and EVs isolated from 29 patients (13 with chronic obstructive pulmonary disease [COPD], four with COPD and asthma, and 12 with asthma; median age 72 years) were analyzed. Based on the Kihon Checklist, patients were classified as frail (n = 11) or non-frail (n = 18). Small RNA sequencing and differential expression analyses were conducted, followed by age-adjusted correlation with physical factors and Ingenuity Pathway Analysis (IPA). A total of 108 small RNAs were differentially expressed between frail and non-frail groups (p < 0.05, fold change < 0.8 or >1.2). IPA linked these RNAs to lung fibrosis and transforming growth factor-beta (TGF-β) signaling pathways. Eleven small RNAs correlated with lower limb strength, and three—miR-125b-5p, miR-369-3p, and miR-615-3p—emerged as key candidates associated with frailty. These findings suggest that EV-derived small RNAs may contribute to frailty development in OPD through TGF-β–related molecular mechanisms. Full article
(This article belongs to the Special Issue Molecular Pathology, Diagnostics, and Therapeutics of Lung Disease)
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18 pages, 2154 KB  
Article
Evaluating the Influence of CHI3L1 and PI3 Methylation in Allergic and Nonallergic Asthma
by Selene Baos, Lucía Cremades-Jimeno, María Ángeles de Pedro, María López-Ramos, Rubén Fernández-Santamaría, Cristina Rosales-Ariza, Joaquín Quiralte, Fernando Florido, Nicolás González-Mangado, María Jesús Rodríguez-Nieto, Germán Peces-Barba, Joaquín Sastre and Blanca Cárdaba
Biomolecules 2025, 15(10), 1363; https://doi.org/10.3390/biom15101363 - 25 Sep 2025
Viewed by 684
Abstract
Previously, we defined CHI3L1 and PI3 as genes related with asthma and severity by analysis of differential gene expression. In this study, we investigated the role of DNA methylation in their regulation, and their relationship with protein levels and clinical parameters. Peripheral blood [...] Read more.
Previously, we defined CHI3L1 and PI3 as genes related with asthma and severity by analysis of differential gene expression. In this study, we investigated the role of DNA methylation in their regulation, and their relationship with protein levels and clinical parameters. Peripheral blood mononuclear cells (PBMCs) and sera were collected from healthy controls (HCs), nonallergic asthmatic (NA), and allergic asthmatic (AA) patients. RNA and DNA were extracted from PBMCs using the trizol method. Gene expression was assessed by qRT-PCR, and DNA methylation of CpG sites near the promoters was analyzed using sodium bisulfite treatment followed by PCR amplification. DNA methylation analysis was performed using the Sequenom EpiTYPER platform. Protein levels were quantified by ELISA, and statistical analyses were carried out using GraphPad software. Consistent with previous findings, CHI3L1 and PI3 gene expression were significantly lower in asthmatic patients compared to controls. Conversely, CHI3L1 protein levels were higher in both patient groups, while PI3 protein showed no significant changes. DNA methylation analysis revealed higher overall DNA methylation percentages in NA and AA patients for both genes compared to HCs. Despite this, no significant correlations were observed between DNA methylation and gene or protein expression, although some correlations were observed with clinical parameters. In conclusion, CHI3L1 and PI3 represent potential asthma biomarkers, whose regulation may be partially influenced by DNA methylation, a mechanism more pronounced in asthmatic patients than in healthy subjects. Full article
(This article belongs to the Special Issue Molecular Pathology, Diagnostics, and Therapeutics of Lung Disease)
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Review

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21 pages, 939 KB  
Review
Recent Advances in the Development and Clinical Use of HER2 Inhibitors in Non-Small Cell Lung Cancer
by Richy Ekyalongo, Toshimitsu Yamaoka and Junji Tsurutani
Biomolecules 2025, 15(10), 1443; https://doi.org/10.3390/biom15101443 - 12 Oct 2025
Viewed by 2519
Abstract
Alterations in the human epidermal growth factor receptor 2 (HER2) gene are well-recognized oncogenic drivers and therapeutic targets in non-small cell lung cancer (NSCLC). The first anti-HER2 inhibitor, trastuzumab-deruxtecan, was approved for previously treated advanced NSCLC with HER2 mutations, which accounts [...] Read more.
Alterations in the human epidermal growth factor receptor 2 (HER2) gene are well-recognized oncogenic drivers and therapeutic targets in non-small cell lung cancer (NSCLC). The first anti-HER2 inhibitor, trastuzumab-deruxtecan, was approved for previously treated advanced NSCLC with HER2 mutations, which accounts for 2–4% of NSCLC. The first anti-HER2 antibody, trastuzumab, was approved for HER2-positive metastatic breast cancer in 1998, and a combination therapy comprising trastuzumab, pertuzumab, and docetaxel demonstrated efficacy in the first-line setting. Some EGFR-tyrosine kinase inhibitors (TKIs) have been evaluated as pan-HER TKIs but have shown limited benefits in HER2-altered NSCLC. However, HER2-specific TKIs, such as zongertinib and BAY2927088, have demonstrated encouraging results. Zongertinib was the first HER2-specific TKI to be approved by the FDA in 2025 for previously treated ERBB2-mutated advanced NSCLC. In this narrative review, we have summarized the latest research on the biology of HER2 signaling, HER2 alterations, HER2-targeting therapies, and challenges of treating HER2-overexpressing or -mutated NSCLC. Despite different targets of HER2 mutations in NSCLC and HER2 amplification/overexpression in breast cancer, the development of HER2-targeting agents has been more advanced in breast cancer than in NSCLC. Therefore, pivotal clinical studies in breast cancer may help in identifying more effective therapies for NSCLC. Full article
(This article belongs to the Special Issue Molecular Pathology, Diagnostics, and Therapeutics of Lung Disease)
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