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Medicina
Special Issues
Pulmonary Fibrosis: Current Understanding and Future Directions
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Pulmonary Fibrosis: Current Understanding and Future Directions

A special issue of Medicina (ISSN 1648-9144). This special issue belongs to the section "Pulmonology".

Deadline for manuscript submissions: 25 October 2025 | Viewed by 424

Special Issue Editors

Dr. Satoshi Okamori

E-Mail Website
Guest Editor
1. Division of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan
2. Pulmonary Division, Department Internal Medicine, Saiseikai Utsunomiya Hospital, Tochigi, Japan
Interests: respiratory; pulmonary disease; interstitial lung
Dr. Yusuke Nakamura

E-Mail Website
Guest Editor
Department of Pulmonary Medicine and Clinical Immunology, Dokkyo Medical University School of Medicine, Mibu 321-0293, Japan
Interests: vascular endothelial cells and pulmonary fibrosis; lipid metabolism in asthma and interstitial pneumonia; regenerative medicine

Special Issue Information

Dear Colleagues,

This Special Issue, entitled “Pulmonary Fibrosis: Current Understanding and Future Directions”, aims to explore the multifaceted nature of interstitial lung disease (ILD) and pulmonary fibrosis, including the pathogenesis, diagnosis, and management of a wide array of inflammatory and fibrotic lung diseases. ILDs encompass a diverse group of disorders, ranging from idiopathic pulmonary fibrosis (IPF) to hypersensitivity pneumonitis, collagen tissue disease-associated ILDs, and drug-induced ILDs. Despite advances in pharmacotherapy, achieving adequate symptom control remains challenging, highlighting the need for a holistic approach that includes nutrition, rehabilitation, and innovative diagnostic techniques.

We invite submissions on a wide range of topics, including, but not limited to, the following: unclassifiable ILDs, fibrotic hypersensitivity pneumonitis, acute exacerbations, pleuroparenchymal fibroelastosis, severe immune-related adverse events in ILDs, and rehabilitation and nutrition in patients with ILDs. Additionally, we welcome research on emerging diagnostic tools, such as bronchoscopy with cryobiopsy, and novel therapeutic strategies, which are becoming increasingly important in the field.
With anticipation, we invite you to submit original research articles or reviews and other types of articles to this Special Issue. Your contributions will promote intellectual collaboration in the field of ILD, ultimately improving patient outcomes and guiding future research directions.

Dr. Satoshi Okamori
Dr. Yusuke Nakamura
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. Medicina is an international peer-reviewed open access monthly 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 2200 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
  • interstitial lung disease (ILD)
  • idiopathic pulmonary fibrosis (IPF)
  • hypersensitivity pneumonitis
  • bronchoscopy
  • cryobiopsy
  • fibrotic lung disease
  • acute exacerbations
  • pleuroparenchymal fibroelastosis
  • rehabilitation
  • nutrition

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Published Papers (1 paper)

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Research

13 pages, 7485 KiB  
Article
Saroglitazar Ameliorates Pulmonary Fibrosis Progression in Mice by Suppressing NF-κB Activation and Attenuating Macrophage M1 Polarization
by Yawen Zhang, Jiaquan Lin, Xiaodong Han and Xiang Chen
Medicina 2025, 61(7), 1157; https://doi.org/10.3390/medicina61071157 - 26 Jun 2025
Viewed by 250
Abstract
Background and Objectives: Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial lung disease with limited therapeutic options. Current therapies (pirfenidone, nintedanib) exhibit modest efficacy and significant side effects, underscoring the need for novel strategies targeting early pathogenic drivers. Saroglitazar (SGZ), [...] Read more.
Background and Objectives: Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial lung disease with limited therapeutic options. Current therapies (pirfenidone, nintedanib) exhibit modest efficacy and significant side effects, underscoring the need for novel strategies targeting early pathogenic drivers. Saroglitazar (SGZ), a dual PPARα/γ agonist with anti-inflammatory properties approved for diabetic dyslipidemia, has not been explored for IPF. We aimed to investigate SGZ’s therapeutic potential in pulmonary fibrosis and elucidate its mechanisms of action. Materials and Methods: Using a bleomycin (BLM)-induced murine pulmonary fibrosis model, we administered SGZ therapeutically. A histopathological assessment (H&E, Masson’s trichrome, collagen I immunofluorescence), Western blotting, and qRT-PCR analyzed the fibrosis progression and inflammatory markers. Flow cytometry evaluated the macrophage polarization. In vitro studies used RAW264.7 macrophages stimulated with BLM/LPS and MRC-5 fibroblast co-cultures. The NF-κB/NLRP3 pathway activation was assessed through protein and gene expression. Results: SGZ significantly attenuated BLM-induced histopathological hallmarks, including alveolar wall thickening, collagen deposition, and inflammatory infiltration. Fibrotic markers (OPN, α-SMA) and pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) were downregulated in the SGZ-treated mice. Mechanistically, SGZ suppressed the M1 macrophage polarization (reduced CD86+ populations) and inhibited the NF-κB/NLRP3 pathway activation in the alveolar macrophages. In the RAW264.7 cells, SGZ decreased the NLRP3 inflammasome components (ASC, cleaved IL-1β) and cytokine secretion. Co-cultures demonstrated that the SGZ-treated macrophage supernatants suppressed the fibroblast activation (α-SMA, collagen I) in MRC-5 cells. Conclusions: SGZ attenuates pulmonary fibrosis by suppressing macrophage-driven inflammation via NF-κB/NLRP3 inhibition and disrupting the macrophage–fibroblast crosstalk. These findings nominate SGZ as a promising candidate for preclinical optimization and future clinical evaluation in IPF. Full article
(This article belongs to the Special Issue Pulmonary Fibrosis: Current Understanding and Future Directions)
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