Topic Editors

1. Department of Experimental Pathology, Institut d'Investigacions Biomèdiques de Barcelona, Consejo Superior de Investigaciones Científicas, Institut d'Investigacions Biomédiques August Pi i Sunyer, Barcelona, Spain
2. Biomedical Research Networking Center in Respiratory Diseases (CIBERES), Madrid, Spain
Department of Experimental Pathology, Institut d'Investigacions Biomèdiques de Barcelona, Consejo Superior de Investigaciones Científicas, Institut d'Investigacions Biomédiques August Pi i Sunyer, 08036 Barcelona, Spain
Department of Pulmonary Medicine, Dr. Josep Trueta University Hospital de Girona, Santa Caterina Hospital de Salt and the Girona Biomedical Research Institut (IDIBGI), 17190 Girona, Spain

Pulmonary Fibrosis and Cell Therapy

Abstract submission deadline
closed (8 March 2023)
Manuscript submission deadline
closed (8 July 2023)
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3692

Topic Information

Dear Colleagues,

During these last two decades, cell therapies for the treatment of pulmonary fibrosis have been considered a promising treatment. In that time, different types of stem cells or lung progenitor cells have been evaluated, mostly in animal models and only in a few human clinical trials. However, although both preclinical and human clinical data support the safety of cell therapies, they have not been translated into routine clinical practice. The reasons are diverse, since many key unanswered questions remain, such as doubts about the type of cells to be transplanted, the origin of these cells (autologous or heterologous), the route of administration (intravenous or endotracheal), the dose, the best time for transplantation, and others. Additionally, the concern about side effects, such as unwanted differentiation of the grafted stem cells, cannot be ignored. In addition to answering these questions, it is essential to know the mechanisms by which cell therapies exert their positive effects. Recent studies indicate that most positive effects can be attributed to the cellular secretome, composed of free soluble proteins and extracellular vesicles. The use of the secretome would avoid the side effects associated with cells, as well as the difficulty in obtaining and expanding them. Therefore, it is not only important to answer these questions, but also to know the mechanisms by which cell therapies exert their positive effects. All of this knowledge would help to consolidate cell therapies in clinical practice. This Topic aims to summarize the updated knowledge on different cell therapies and the mechanisms involved in their potential therapeutic effect in pulmonary fibrosis. The Topic, entitled “Pulmonary Fibrosis and Cell Therapy”, will include both review and original research papers covering key topics related to different cell therapies for pulmonary fibrosis, such as:
(1) different types of stem cells, induced pluripotent stem cells (iPSC), non-derived and derived from pulmonary cells;
(2) lung progenitor cells;
(3) other type of pulmonary cells;
(4) the cell secretome;
(5) cell–cell interactions;
(6) investigation of mechanisms of lung tissue regeneration, cell engraftment, or the cell secretome.

We hope that our readers from various disciplines will benefit from this Topic, which will serve as a gateway to the amazing world of cell therapies for fibrotic diseases. We look forward to your contributions.

Dr. Victor Ivo Peinado
Dr. Anna Serrano-Mollar
Dr. Olga Tura-Ceide
Topic Editors

Participating Journals

Journal Name Impact Factor CiteScore Launched Year First Decision (median) APC
Biomolecules
biomolecules
5.5 8.3 2011 16.9 Days CHF 2700
Cells
cells
6.0 9.0 2012 16.6 Days CHF 2700
International Journal of Molecular Sciences
ijms
5.6 7.8 2000 16.3 Days CHF 2900
Journal of Molecular Pathology
jmp
- - 2020 24.9 Days CHF 1000
Organoids
organoids
- - 2022 15.0 days * CHF 1000

* Median value for all MDPI journals in the second half of 2023.


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Published Papers (1 paper)

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15 pages, 3858 KiB  
Article
Invadosome Formation by Lung Fibroblasts in Idiopathic Pulmonary Fibrosis
by Mégane Lebel, Dominic O. Cliche, Martine Charbonneau, Damien Adam, Emmanuelle Brochiero, Claire M. Dubois and André M. Cantin
Int. J. Mol. Sci. 2023, 24(1), 499; https://doi.org/10.3390/ijms24010499 - 28 Dec 2022
Cited by 2 | Viewed by 2285
Abstract
Idiopathic pulmonary fibrosis (IPF) is characterized by abnormal fibroblast accumulation in the lung leading to extracellular matrix deposition and remodeling that compromise lung function. However, the mechanisms of interstitial invasion and remodeling by lung fibroblasts remain poorly understood. The invadosomes, initially described in [...] Read more.
Idiopathic pulmonary fibrosis (IPF) is characterized by abnormal fibroblast accumulation in the lung leading to extracellular matrix deposition and remodeling that compromise lung function. However, the mechanisms of interstitial invasion and remodeling by lung fibroblasts remain poorly understood. The invadosomes, initially described in cancer cells, consist of actin-based adhesive structures that coordinate with numerous other proteins to form a membrane protrusion capable of degrading the extracellular matrix to promote their invasive phenotype. In this regard, we hypothesized that invadosome formation may be increased in lung fibroblasts from patients with IPF. Public RNAseq datasets from control and IPF lung tissues were used to identify differentially expressed genes associated with invadosomes. Lung fibroblasts isolated from bleomycin-exposed mice and IPF patients were seeded with and without the two approved drugs for treating IPF, nintedanib or pirfenidone on fluorescent gelatin-coated coverslips for invadosome assays. Several matrix and invadosome-associated genes were increased in IPF tissues and in IPF fibroblastic foci. Invadosome formation was significantly increased in lung fibroblasts isolated from bleomycin-exposed mice and IPF patients. The degree of lung fibrosis found in IPF tissues correlated strongly with invadosome production by neighboring cells. Nintedanib suppressed IPF and PDGF-activated lung fibroblast invadosome formation, an event associated with inhibition of the PDGFR/PI3K/Akt pathway and TKS5 expression. Fibroblasts derived from IPF lung tissues express a pro-invadosomal phenotype, which correlates with the severity of fibrosis and is responsive to antifibrotic treatment. Full article
(This article belongs to the Topic Pulmonary Fibrosis and Cell Therapy)
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