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Cells
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Mechanisms of Lung Growth and Regeneration
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Mechanisms of Lung Growth and Regeneration

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Microenvironment".

Deadline for manuscript submissions: 31 July 2026 | Viewed by 8178

Special Issue Editors

Prof. Dr. Saverio Bellusci

E-Mail Website
Guest Editor
Medical Clinic and Polyclinic II Pneumology, Gastroenterology, Nephrology and Internal Intensive Care Medicine Clinic, University Hospital Giessen and Marburg, Street 33, 35392 Giessen, Germany
Interests: lung development and regeneration/repair; fibroblast growth factors; epithelial stem cells; resident stromal niche; lipofibroblasts; fibrosis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Yuanlin Song

E-Mail Website
Guest Editor
Department of Pulmonary and Critical Care Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, China
Interests: acute respiratory distress syndrome; mortality; diagnosis; prognosis; treatment; clinical trial

Special Issue Information

Dear Colleagues,

Lung growth and regeneration are governed by epithelial–mesenchymal–vascular–immune cell interactions. The signaling pathways involved in lung growth are also recapitulated during regeneration following injury. This Special Issue will focus on understanding key cellular and molecular processes underlying lung growth and regeneration in the context of age, environment and species, with the hope of better understanding disease development; this constitutes the basis to establish novel regenerative approaches.

This Special Issue will highlight critical aspects of lung epithelial biology such as stem cells and regenerative medicine. The different epithelial stem/progenitor cells identified in the different regions of the lung interact with specific mesenchymal, immune and vascular niches that have recently been characterized. These niches dictate the quiescence of the epithelial stem/progenitor cells, their re-entry into the cell cycle and subsequent differentiation, as well as their regenerative potential. Emerging studies have shed light on the cells composing these different niches and their distinct roles in driving development, homeostasis, injury/repair and disease development

The biological distinctions between mesenchymal proliferation as a repair mechanism and fibrosis will also be of interest. Studies and reviews aiming to describe new tools in single-cell analysis, allowing a better understanding of lung development and regeneration, are welcomed. Research on the characterization of epithelial–mesenchymal interrelationships that maintain lung homeostasis and orchestrate growth and regeneration is also welcomed.

Prof. Dr. Saverio Bellusci
Prof. Dr. Yuanlin Song
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 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. 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

  • stem cells
  • niche
  • aging
  • growth factors
  • extracellular matrix
  • organoids
  • fibrosis
  • single-cell RNAseq

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Published Papers (4 papers)

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Review

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22 pages, 2780 KB  
Review
Hippo Signaling in the Lung: A Tale of Two Effectors—Yap Drives Airway Fate and Taz Drives Alveolar Differentiation
by Rachel Warren and Stijn P. J. De Langhe
Cells 2026, 15(2), 143; https://doi.org/10.3390/cells15020143 - 13 Jan 2026
Cited by 1 | Viewed by 1379
Abstract
The mammalian lung operates under a biological paradox, requiring architectural fragility for gas exchange while maintaining robust regenerative plasticity to withstand injury. The Hippo signaling pathway has emerged as a central “rheostat” in orchestrating these opposing needs, yet the distinct roles of its [...] Read more.
The mammalian lung operates under a biological paradox, requiring architectural fragility for gas exchange while maintaining robust regenerative plasticity to withstand injury. The Hippo signaling pathway has emerged as a central “rheostat” in orchestrating these opposing needs, yet the distinct roles of its downstream effectors remain underappreciated. This review synthesizes recent genetic and mechanobiological advances to propose a “Tale of Two Effectors” model, arguing for the functional non-redundancy of YAP and TAZ. We posit that YAP functions to drive airway progenitor expansion, mechanical force generation, and maladaptive remodeling. Conversely, TAZ—regulated uniquely via transcriptional mechanisms and mechanotransduction—acts as an obligate driver of alveolar differentiation and adaptive repair through an NKX2-1 feed-forward loop. Furthermore, we introduce the “See-Saw” model of tissue fitness, where mesenchymal niche collapse releases the mechanical brake on the epithelium, triggering the bronchiolization characteristic of pulmonary fibrosis. Finally, we extend this framework to malignancy, illustrating how Small Cell Lung Cancer (SCLC) subtypes mirror these developmental and regenerative states. This integrated framework offers new therapeutic distinct targets for modulating tissue fitness and resolving fibrosis. Full article
(This article belongs to the Special Issue Mechanisms of Lung Growth and Regeneration)
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31 pages, 1965 KB  
Review
Reciprocal Paracrine Signaling and Dynamic Coordination of Transitional States in the Alveolar Epithelial Type 2 Cells and Associated Alveolar Lipofibroblasts During Homeostasis, Injury and Repair
by Georgios-Dimitrios Panagiotidis, Mengqing Chen, Xiuyue Yang, Manuela Marega, Stefano Rivetti, Xuran Chu and Saverio Bellusci
Cells 2025, 14(23), 1869; https://doi.org/10.3390/cells14231869 - 26 Nov 2025
Cited by 1 | Viewed by 1593
Abstract
Single-cell RNA-sequencing has transformed our understanding of alveolar epithelial type 2 (AT2) cells and alveolar lipofibroblasts (LIFs) during lung injury and repair. Both cell types undergo dynamic transitions through intermediate states that determine whether the lung proceeds toward regeneration or fibrosis. Emerging evidence [...] Read more.
Single-cell RNA-sequencing has transformed our understanding of alveolar epithelial type 2 (AT2) cells and alveolar lipofibroblasts (LIFs) during lung injury and repair. Both cell types undergo dynamic transitions through intermediate states that determine whether the lung proceeds toward regeneration or fibrosis. Emerging evidence highlights reciprocal paracrine signaling between AT2/AT1 transitional cells and LIF-derived myofibroblasts (aMYFs) as a key regulatory axis. Among these, amphiregulin (AREG)–EGFR signaling functions as a central profibrotic pathway whose inhibition can restore alveolar differentiation and repair. The human WI-38 fibroblast model provides a practical platform to study the reversible LIF–MYF switch and screen antifibrotic and pro-regenerative compounds. Candidate therapeutics including metformin, haloperidol and FGF10 show promise in reprogramming fibroblast and epithelial states through metabolic and signaling modulation. Integrating WI-38-based assays, alveolosphere co-cultures, and multi-omics profiling offers a translational framework for identifying interventions that halt fibrosis and actively induce lung regeneration. This review highlights a unifying framework in which epithelial and mesenchymal plasticity converge to define repair outcomes and identifies actionable targets for promoting alveolar regeneration in chronic lung disease. Full article
(This article belongs to the Special Issue Mechanisms of Lung Growth and Regeneration)
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25 pages, 2127 KB  
Review
Fibroblast Growth Factors in Lung Development and Regeneration: Mechanisms and Therapeutic Potential
by Karolina Baran, Kamila Skrzynska, Aleksandra A. Czyrek, Adrianna Wittek, Daniel Krowarsch, Anna Szlachcic, Malgorzata Zakrzewska and Julia Chudzian
Cells 2025, 14(16), 1256; https://doi.org/10.3390/cells14161256 - 14 Aug 2025
Cited by 5 | Viewed by 4493
Abstract
Fibroblast growth factors (FGFs) play a key role in lung development by mediating complex interactions between epithelial and mesenchymal cells, which are central to processes such as branching morphogenesis, epithelial differentiation, and alveolarization. The findings regarding this interplay highlight the complexity of FGF [...] Read more.
Fibroblast growth factors (FGFs) play a key role in lung development by mediating complex interactions between epithelial and mesenchymal cells, which are central to processes such as branching morphogenesis, epithelial differentiation, and alveolarization. The findings regarding this interplay highlight the complexity of FGF signaling, as different FGFs contribute to various aspects of lung formation and maturation. Understanding the role of FGF proteins in shaping the lung is crucial for gaining insight into the biology of its development. Furthermore, FGFs orchestrate complex signaling pathways that regulate lung regeneration in adulthood. Therapeutic strategies targeting FGF-dependent pathways appear promising for repairing and improving lung function in diverse pulmonary diseases. In this review, we describe the current perception of the role of FGF proteins in lung development and regeneration, together with an overview of emerging therapeutic strategies aiming at FGF signaling in lung-related disorders. Full article
(This article belongs to the Special Issue Mechanisms of Lung Growth and Regeneration)
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Other

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14 pages, 2723 KB  
Technical Note
Spatial Protein Expression Analysis in Lungs Using Capillary-Based Immunoassay After Laser-Assisted Microdissection
by Stefan Hadzic, Marija Gredic, Vanessa Nebel, Norbert Weissmann and Cheng-Yu Wu
Cells 2026, 15(8), 737; https://doi.org/10.3390/cells15080737 - 21 Apr 2026
Viewed by 208
Abstract
Unravelling the cellular and molecular mechanisms underlying lung injury and repair requires precise spatial context. Profiling cell-to-cell transcriptional variability and spatial orientation has become increasingly sophisticated, but validating results at the protein level still remains challenging, particularly for low-expressed proteins or small-scale samples. [...] Read more.
Unravelling the cellular and molecular mechanisms underlying lung injury and repair requires precise spatial context. Profiling cell-to-cell transcriptional variability and spatial orientation has become increasingly sophisticated, but validating results at the protein level still remains challenging, particularly for low-expressed proteins or small-scale samples. Here, we present a workflow established by our group for spatial protein analysis in the lung by combining two commercially available platforms: (1) laser-assisted microdissection (LMD) with (2) a capillary electrophoretic-based immunoassay (CEI). Using this workflow, we demonstrate a simple, accessible, and sensitive method for spatially capturing regions of interest to investigate small-scale samples or low-expressed proteins. This workflow provides an additional option for orthogonal validation for researchers using omics-based approaches. Furthermore, we validated transcriptome analysis results at the protein level by applying this workflow to a pre-clinical model of cigarette smoke (CS)-induced lung injury. In line with the previous findings, the results showed a significant downregulation of the endothelial cell marker in LMD-enriched alveolar regions, suggesting spatial capillary rarefaction, and activation of the mitogen-activated protein kinase (MAPK) signalling pathway in pulmonary vasculature of CS-exposed mice. Our approach overcomes traditional challenges and provides new opportunities for understanding complex disease pathomechanisms and identifying potential therapeutic targets. Full article
(This article belongs to the Special Issue Mechanisms of Lung Growth and Regeneration)
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