Lung Diseases: From Cellular and Molecular Mechanisms to Targeted Therapies

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

Deadline for manuscript submissions: 15 October 2026 | Viewed by 2059

Special Issue Editors


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Guest Editor
Department of Internal Medicine V-Pulmonology, Allergology, Respiratory and Environmental Medicine, Saarland University, 66424 Homburg, Germany
Interests: airway diseases
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Experimental Pharmacology, Center for Molecular Signaling (PZMS), School of Medicine, Saarland University, 66421 Homburg, Germany
Interests: airway diseases

Special Issue Information

Dear Colleagues,

Lung diseases such as pneumonia, asthma, chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis and cystic fibrosis affect hundreds of millions of people worldwide, profoundly affecting quality of life and substantially contributing to mortality. Impaired lung function is central to these conditions, typically resulting from a pathogenesis involving acute and chronic inflammation, tissue destruction and airway remodelling. As many lung diseases are incurable and often fatal, with current therapies primarily offering symptomatic relief, it is crucial to gain a deeper understanding of the underlying cellular and molecular mechanisms of these diseases.

Emerging technologies, including 3D organoid cultures, single-cell sequencing, spatial transcriptomics and single-cell epigenomics, now offer unparalleled opportunities to analyse disease pathways and reveal new therapeutic targets. By bridging the gap between fundamental biology and clinical application, these approaches offer great potential for developing mechanism-based therapies.

We invite authors to contribute their work to this Special Issue, “Lung Diseases: From Cellular and Molecular Mechanisms to Targeted Therapies”. We welcome original research articles, reviews and methodological studies that enhance our understanding of the complexity of airway diseases. Topics may include, but are not limited to, the mechanisms driving inflammation, tissue destruction, airway remodelling and therapies. Submissions with clear translational relevance are particularly encouraged.

Prof. Dr. Christoph Beisswenger
Prof. Dr. Daniela Yildiz
Guest Editors

Manuscript Submission Information

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Keywords

  • lung diseases
  • cellular and molecular mechanisms
  • targeted therapies
  • OMICS
  • single-cell sequencing

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Published Papers (1 paper)

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Review

28 pages, 6012 KB  
Review
TGF-β Signaling as a Pathological Continuum Linking Idiopathic Pulmonary Fibrosis and Lung Cancer
by Kuo-Liang Huang, Lu-Kai Wang and Fu-Ming Tsai
Cells 2026, 15(5), 480; https://doi.org/10.3390/cells15050480 - 6 Mar 2026
Cited by 1 | Viewed by 1676
Abstract
Transforming growth factor-β (TGF-β) signaling plays a central role in lung tissue homeostasis, coordinating epithelial repair, immune resolution, and stromal remodeling following injury. However, persistent or dysregulated TGF-β activation is a hallmark of both idiopathic pulmonary fibrosis (IPF) and lung cancer, two devastating [...] Read more.
Transforming growth factor-β (TGF-β) signaling plays a central role in lung tissue homeostasis, coordinating epithelial repair, immune resolution, and stromal remodeling following injury. However, persistent or dysregulated TGF-β activation is a hallmark of both idiopathic pulmonary fibrosis (IPF) and lung cancer, two devastating pulmonary diseases that are traditionally studied as distinct entities. Emerging evidence suggests that this dichotomous view may obscure shared pathogenic mechanisms driven by aberrant TGF-β signaling dynamics. In this review, we synthesize experimental, translational, and clinical findings to propose a unifying framework in which IPF and lung cancer represent endpoints along a shared TGF-β–driven pathological continuum. We highlight how the duration and intensity of TGF-β signaling determine divergent cellular outcomes across epithelial cells, fibroblasts, and immune compartments—ranging from physiological wound repair to irreversible fibrotic remodeling and the establishment of a pro-tumorigenic niche. Particular emphasis is placed on the temporal transition from acute injury responses to chronic signaling states that promote epithelial plasticity, fibroblast fixation, immune suppression, and genomic instability. By integrating fibrosis and tumorigenesis into a single pathophysiological model, this review reframes TGF-β signaling as a time-dependent disease modifier rather than a disease-specific factor. This perspective provides a conceptual basis for therapeutic strategies targeting TGF-β signaling windows to intercept disease progression before irreversible fibrosis or malignant transformation occurs. Full article
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