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Cells
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Mechanisms of Respiratory Diseases
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Mechanisms of Respiratory Diseases

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

Deadline for manuscript submissions: closed (31 May 2025) | Viewed by 6225

Special Issue Editors

Prof. Dr. Bernhard Ryffel

E-Mail Website
Guest Editor
CNRS, INEM, UMR7355, University of Orleans, 45071 Orleans, France
Interests: injury-induced inflammation; chronic progressive respiratory diseases; viral superinfection; innate immune danger sensing; cGAS/STING; inflammasome activation; IL-1 family; Th2; Th17; altered microbiota; metabolites; tissue homeostasis; inflammatory responses; translational research in mouse models of human disease
Special Issues, Collections and Topics in MDPI journals
Dr. David Rios-Covián

E-Mail Website
Guest Editor
Microviable Therapeutics S.L., Oviedo, Asturias, Spain
Interests: host-microbiome interactions in the context of health and disease; development of microbiome-based therapies and biological drugs; bacterial metabolites and their interactions with the host's immune system, with a special focus on products of bacterial fermentation such as short-chain fatty acids and branched short-chain fatty acids

Special Issue Information

Dear Colleagues,

Understanding the mechanisms of respiratory diseases related to environmental exposure is a major challenge. The focus of this Special Issue is on the research of stressors such as particles, smoke, ozone or other inhaled agents activating inflammatory pathways and non-resolving, progressive lung destruction and fibrosis and exacerbation by viral infections. Contributions are invited that help to understand the role of innate receptors such as TLR, NLRP, cGAS/STING, ferroptosis, autophagy, senescence or cytokines such as IL-1, TNF and FASL to elicit host innate immune responses leading to inflammatory diseases.

The interplay between altered microbiota composition and metabolites linked to inflammation is a factor to be considered in pathogenesis. Translational contributions including defined inhibitors in rodents and human cell culture are of interest, and recent discoveries for this thematic issue of Cells are welcome.

Prof. Dr. Bernhard Ryffel
Dr. David Rios-Covián
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 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. 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

  • cell death/stress
  • DNA/RNA sensor
  • cGAS/STING
  • inflammasome
  • microbiome
  • FMT or transfer of bacteria
  • metabolite
  • viral infection
  • emphysema
  • progressive fibrosis
  • innate immune response
  • defined inhibitors

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Published Papers (2 papers)

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Research

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29 pages, 3538 KB  
Article
Mitochondrial Fragmentation Induced by the CFTR Modulators Lumacaftor and Ivacaftor in Immortalized Cystic Fibrosis Cell Lines
by Camila Dib, Pablo A. Iglesias González, María de los Ángeles Aguilar, Guillermo L. Taminelli, Tatiana Limpias del Valle, Nadia E. Nuñez, Analía G. Karadayian, Tomás A. Santa-Coloma and Ángel G. Valdivieso
Cells 2025, 14(20), 1601; https://doi.org/10.3390/cells14201601 - 15 Oct 2025
Viewed by 928
Abstract
Cystic fibrosis (CF) is an autosomal recessive disease caused by mutations in the CFTR gene, which encodes a cAMP-activated chloride channel essential for epithelial function. Beyond its canonical role, evidence suggests CFTR also influences mitochondrial function. Previous studies have identified CFTR- and Cl-dependent [...] Read more.
Cystic fibrosis (CF) is an autosomal recessive disease caused by mutations in the CFTR gene, which encodes a cAMP-activated chloride channel essential for epithelial function. Beyond its canonical role, evidence suggests CFTR also influences mitochondrial function. Previous studies have identified CFTR- and Cl-dependent genes, including MTND4 and CISD1, which are downregulated in CF cells and play a critical role in mitochondrial function. CF cells exhibit altered mitochondrial complex I (mCx-I) activity and impaired electron transport chain function, although the underlying mechanisms remain unclear. In this study, the impact of the CFTR modulators lumacaftor (VX-809) and ivacaftor (VX-770) on mitochondrial morphology and function was investigated in heterozygous ΔF508/W1282X CF IB3-1 cells. Combined treatment with VX-809 (10 μM, CFTR corrector) and VX-770 (0.1 μM, CFTR potentiator) induced a fragmented mitochondrial morphology in both CF and CF expressing wt-CFTR cells, without affecting cell viability or mitochondrial membrane potential (ΔΨm). While individual treatments differentially modulated ROS production and ΔΨm, these effects were not statistically significant under combined treatment. These results highlight a previously unrecognized role for CFTR modulators in shaping mitochondrial morphology. A better understanding of these effects may reveal novel mechanisms underlying the regulation of mitochondrial structure and function. Full article
(This article belongs to the Special Issue Mechanisms of Respiratory Diseases)
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Review

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18 pages, 982 KB  
Review
Unlocking the Future: Pluripotent Stem Cell-Based Lung Repair
by Tobias Goecke, Fabio Ius, Arjang Ruhparwar and Ulrich Martin
Cells 2024, 13(7), 635; https://doi.org/10.3390/cells13070635 - 5 Apr 2024
Cited by 3 | Viewed by 4718
Abstract
The human respiratory system is susceptible to a variety of diseases, ranging from chronic obstructive pulmonary disease (COPD) and pulmonary fibrosis to acute respiratory distress syndrome (ARDS). Today, lung diseases represent one of the major challenges to the health care sector and represent [...] Read more.
The human respiratory system is susceptible to a variety of diseases, ranging from chronic obstructive pulmonary disease (COPD) and pulmonary fibrosis to acute respiratory distress syndrome (ARDS). Today, lung diseases represent one of the major challenges to the health care sector and represent one of the leading causes of death worldwide. Current treatment options often focus on managing symptoms rather than addressing the underlying cause of the disease. The limitations of conventional therapies highlight the urgent clinical need for innovative solutions capable of repairing damaged lung tissue at a fundamental level. Pluripotent stem cell technologies have now reached clinical maturity and hold immense potential to revolutionize the landscape of lung repair and regenerative medicine. Meanwhile, human embryonic (HESCs) and human-induced pluripotent stem cells (hiPSCs) can be coaxed to differentiate into lung-specific cell types such as bronchial and alveolar epithelial cells, or pulmonary endothelial cells. This holds the promise of regenerating damaged lung tissue and restoring normal respiratory function. While methods for targeted genetic engineering of hPSCs and lung cell differentiation have substantially advanced, the required GMP-grade clinical-scale production technologies as well as the development of suitable preclinical animal models and cell application strategies are less advanced. This review provides an overview of current perspectives on PSC-based therapies for lung repair, explores key advances, and envisions future directions in this dynamic field. Full article
(This article belongs to the Special Issue Mechanisms of Respiratory Diseases)
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