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Molecular Perspectives in Lung Diseases: Pathogenesis, Diagnosis, and Treatment
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Molecular Perspectives in Lung Diseases: Pathogenesis, Diagnosis, 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: 20 November 2025 | Viewed by 1848

Special Issue Editor

Dr. Elena Levantini

E-Mail Website
Guest Editor
Consiglio Nazionale delle Ricerche, Istituto di Tecnologie Biomediche, via Moruzzi 1, 56124 Pisa, Italy
Interests: NSCLC; SCLC; murine models; tumor microenvironment; cancer stem cells; therapy resistance; therapeutic targeting; BMI1; scRNAseq; spatial transcriptomics; single-cell interactomes; gene regulation; transcription factors; KRAS; EGFR; miRNA
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue focuses on the intricate molecular mechanisms underlying lung diseases, with a focus on pathogenesis, diagnosis, and treatment. We aim to explore cutting-edge research on lung cancer models, cancer stem cells, and the tumor microenvironment. Key topics include the development and application of targeted therapies, particularly in the context of non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC).

Our interests span a wide array of molecular and cellular aspects, including the role of BMI1 in cancer stem cell regulation, the use of murine models to study disease progression and resistance to therapy, and the application of single-cell RNA sequencing (scRNAseq) and spatial transcriptomics to uncover novel targeting strategies. We also emphasize the importance of gene regulation, transcription factors, miRNAs, single-cell interaction networks, as well as KRAS and EGFR mutations, among others, in lung cancer biology.

By bringing these diverse yet interconnected areas of research together, this Issue aims to provide a comprehensive overview of the current state of lung disease research and highlight the potential personalized medicine options. We invite contributions that offer new perspectives and innovative approaches to understanding and treating lung diseases.

Dr. Elena Levantini
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

  • lung cancer models
  • cancer stem cells
  • tumor microenvironment
  • targeted therapy

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Published Papers (2 papers)

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Research

16 pages, 2718 KiB  
Article
TGF-β Induced by Allergic Lung Inflammation Enhances Os-Teosarcoma Lung Metastasis in a Mouse Comorbidity Model
by Marco J. Sanchez-Rojas, Belen Tirado-Rodriguez, Gabriela Antonio-Andres, Giovanny Soca-Chafre, Daniel D. Hernandez-Cueto, Cesar O. Martinez-Calderon, Mayra Montecillo-Aguado, Juan C. Hernandez-Guerrero, Marco A. Duran-Padilla, Rogelio Hernandez-Pando and Sara Huerta-Yepez
Int. J. Mol. Sci. 2025, 26(11), 5073; https://doi.org/10.3390/ijms26115073 - 24 May 2025
Viewed by 341
Abstract
TGF-β is a central mediator of pulmonary allergic inflammation recently associated with lung metastasis of osteosarcoma. Given the controversial links between cancer and allergic diseases, this study aimed to evaluate the effects of allergic airway inflammation—particularly TGF-β—on osteosarcoma lung metastasis using a comorbidity [...] Read more.
TGF-β is a central mediator of pulmonary allergic inflammation recently associated with lung metastasis of osteosarcoma. Given the controversial links between cancer and allergic diseases, this study aimed to evaluate the effects of allergic airway inflammation—particularly TGF-β—on osteosarcoma lung metastasis using a comorbidity mouse model. Osteosarcoma cells were implanted in BALB/c mice with induced allergic airway inflammation. Lung metastasis was quantified, while PCNA/TGF-β expression was assessed by immunohistochemistry and digital pathology. Bioinformatic analyses of patient datasets compared TGF-β and PCNA expression in metastatic vs. normal tissues, and their association with survival. Mice with allergic inflammation showed increased lung metastases associated with TGF-β production. In patient samples, both TGF-β and PCNA were upregulated in metastatic tissues and correlated with poor overall survival. PCNA was also linked to genes involved in cell proliferation, DNA replication, and repair. Our results show an association between allergic airway inflammation and extensive lung metastasis of osteosarcoma in a comorbidity mouse model with elevated expression of TGF-β and PCNA. Full article
(This article belongs to the Special Issue Molecular Perspectives in Lung Diseases: Pathogenesis, Diagnosis, and Treatment)
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18 pages, 13833 KiB  
Article
Host Serine Proteases and Antiviral Innate Immunity as Potential Therapeutic Targets in Influenza A Virus Infection-Induced COPD Exacerbations
by Haiqing Bai, Melissa Rodas, Longlong Si, Yuncheng Man, Jie Ji, Roberto Plebani, Johnathan D. Mercer, Rani K. Powers, Chaitra Belgur, Amanda Jiang, Sean R. R. Hall, Rachelle Prantil-Baun and Donald E. Ingber
Int. J. Mol. Sci. 2025, 26(6), 2549; https://doi.org/10.3390/ijms26062549 - 12 Mar 2025
Viewed by 1021
Abstract
Lung manifestations of chronic obstructive pulmonary disease (COPD) are often exacerbated by influenza A virus infections; however, the underlying mechanisms remain largely unknown, and hence therapeutic options are limited. Using a physiologically relevant human lung airway-on-a-chip (Airway Chip) microfluidic culture model lined with [...] Read more.
Lung manifestations of chronic obstructive pulmonary disease (COPD) are often exacerbated by influenza A virus infections; however, the underlying mechanisms remain largely unknown, and hence therapeutic options are limited. Using a physiologically relevant human lung airway-on-a-chip (Airway Chip) microfluidic culture model lined with human airway epithelium from COPD or healthy donors interfaced with pulmonary microvascular endothelium, we observed that Airway Chips lined with COPD epithelium exhibit an increased sensitivity to influenza virus infection, as is observed clinically in COPD patients. Differentiated COPD airway epithelial cells display increased inflammatory cytokine production, barrier function loss, and mucus accumulation upon virus infection. Transcriptomic analysis revealed gene expression profiles characterized by upregulation of serine proteases that may facilitate viral entry and downregulation of interferon-related genes associated with antiviral immune responses. Importantly, treatment of influenza virus-infected COPD epithelium with a protease inhibitor, nafamostat, ameliorated the disease phenotype, as evidenced by dampened viral replication, reduced mucus accumulation, and improved tissue barrier integrity. These findings suggest that targeting host serine proteases may represent a promising therapeutic avenue against influenza-afflicted COPD exacerbations. Full article
(This article belongs to the Special Issue Molecular Perspectives in Lung Diseases: Pathogenesis, Diagnosis, and Treatment)
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