Cellular Signaling and Therapeutic Approaches of Pulmonary Fibrosis

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 3189

Special Issue Editor


E-Mail Website
Guest Editor
MM Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA
Interests: pulmonary fibrosis; alveolar macrophage function; myofibroblast differentiation; fibrosis resolution; cell–cell interactions

Special Issue Information

Dear Colleagues,

Fibrosis is a progressive scarring disease that can affect virtually all the organs in the body and is estimated to account for almost half of all deaths in the United States alone. Pulmonary fibrosis exemplifies this disorder due to its poor prognosis and lack of curative treatment. The key pathogenic steps in pulmonary fibrosis involve epithelial cell disruption, myofibroblast differentiation, macrophage activation, and extracellular matrix deposition, and the interactions between these cell types and the molecular pathways behind these mechanisms represent interesting topics of research. Likewise, our knowledge regarding the reversal or resolution of fibrotic pathogenesis is limited and warrants further exploration.

This Special Issue will explore how cellular signaling contributes to pulmonary fibrogenesis and resolution, with the aim of highlighting potential novel therapeutic targets.

Dr. Jennifer Speth
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. 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

  • pulmonary fibrosis
  • resolution
  • cellular interactions

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Review

13 pages, 2899 KiB  
Review
YAP/TAZ Signaling in the Pathobiology of Pulmonary Fibrosis
by Kostas A. Papavassiliou, Amalia A. Sofianidi, Fotios G. Spiliopoulos, Vassiliki A. Gogou, Antonios N. Gargalionis and Athanasios G. Papavassiliou
Cells 2024, 13(18), 1519; https://doi.org/10.3390/cells13181519 - 10 Sep 2024
Cited by 1 | Viewed by 2822
Abstract
Pulmonary fibrosis (PF) is a severe, irreversible lung disease characterized by progressive scarring, with idiopathic pulmonary fibrosis (IPF) being the most prevalent form. IPF’s pathogenesis involves repetitive lung epithelial injury leading to fibroblast activation and excessive extracellular matrix (ECM) deposition. The prognosis for [...] Read more.
Pulmonary fibrosis (PF) is a severe, irreversible lung disease characterized by progressive scarring, with idiopathic pulmonary fibrosis (IPF) being the most prevalent form. IPF’s pathogenesis involves repetitive lung epithelial injury leading to fibroblast activation and excessive extracellular matrix (ECM) deposition. The prognosis for IPF is poor, with limited therapeutic options like nintedanib and pirfenidone offering only modest benefits. Emerging research highlights the dysregulation of the yes-associated protein (YAP)/transcriptional coactivator with PDZ-binding motif (TAZ) signaling pathway as a critical factor in PF. YAP and TAZ, components of the Hippo pathway, play significant roles in cell proliferation, differentiation, and fibrosis by modulating gene expression through interactions with TEA domain (TEAD) transcription factors. The aberrant activation of YAP/TAZ in lung tissue promotes fibroblast activation and ECM accumulation. Targeting the YAP/TAZ pathway offers a promising therapeutic avenue. Preclinical studies have identified potential treatments, such as trigonelline, dopamine receptor D1 (DRD1) agonists, and statins, which inhibit YAP/TAZ activity and demonstrate antifibrotic effects. These findings underscore the importance of YAP/TAZ in PF pathogenesis and the potential of novel therapies aimed at this pathway, suggesting a new direction for improving IPF treatment outcomes. Further research is needed to validate these approaches and translate them into clinical practice. Full article
(This article belongs to the Special Issue Cellular Signaling and Therapeutic Approaches of Pulmonary Fibrosis)
Show Figures

Figure 1

Back to TopTop