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Biomedicines
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Treatment for Pulmonary Fibrosis, Volume II
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Treatment for Pulmonary Fibrosis, Volume II

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 7961

Special Issue Editors

Prof. Dr. Hiroshi Mukae

E-Mail Website
Guest Editor
Department of Respiratory Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan
Interests: Interstitial pneumonia; pulmonary infection
Special Issues, Collections and Topics in MDPI journals
Dr. Noriho Sakamoto

E-Mail Website
Guest Editor
Department of Respiratory Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan
Interests: sarcoidosis; interstitial lung disease; bronchoalveolar lavage; lymphangioleiomyomatosis; lung

Special Issue Information

Dear Colleagues,

Pulmonary fibrosis is characterized by the excessive deposition of extracellular matrices and destruction of the pulmonary parenchyma. The cause or contributing factor of pulmonary fibrosis is often unknown, and some diseases, including idiopathic pulmonary fibrosis, have poor prognosis despite treatment. Recently, progressive fibrosing interstitial lung disease (PF-ILD) or progressive pulmonary fibrosis (PPF) has been advocated to this phenotype, but there are many uncertainties and problems left to be resolved in the term “PF-ILD or PPF”.

This Special Issue, “Pulmonary Fibrosis: From Pathogenesis to Therapeutics”, aims to focus on novel approaches to the pathogenesis, diagnosis and therapeutics of pulmonary fibrosis at basic to clinical levels.

Prof. Dr. Hiroshi Mukae
Dr. Noriho Sakamoto
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. Biomedicines 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 2600 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

  • idiopathic pulmonary fibrosis
  • anti-fibrotic drug
  • progressive fibrosing interstitial lung disease
  • mechanism
  • pathophysiology
  • interstitial lung disease
  • biomarker

Related Special Issue

Published Papers (4 papers)

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Research

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14 pages, 1370 KiB  
Article
Niclosamide Attenuates Inflammation-Associated Profibrotic Responses in Human Subepithelial Lung Myofibroblasts
by Michail Spathakis, Gesthimani Tarapatzi, Eirini Filidou, Leonidas Kandilogiannakis, Evangelos Karatzas, Paschalis Steiropoulos, Dimitrios Mikroulis, George M. Spyrou, Vangelis G. Manolopoulos, George Kolios and Konstantinos Arvanitidis
Biomedicines 2023, 11(7), 2032; https://doi.org/10.3390/biomedicines11072032 - 19 Jul 2023
Viewed by 1573
Abstract
Niclosamide is a commonly used helminthicidic drug for the treatment of human parasitosis by helminths. Recently, efforts have been focusing on repurposing this drug for the treatment of other diseases, such as idiopathic pulmonary fibrosis. Subepithelial lung myofibroblasts (SELMs) isolated from tissue biopsies [...] Read more.
Niclosamide is a commonly used helminthicidic drug for the treatment of human parasitosis by helminths. Recently, efforts have been focusing on repurposing this drug for the treatment of other diseases, such as idiopathic pulmonary fibrosis. Subepithelial lung myofibroblasts (SELMs) isolated from tissue biopsies of patients undergoing surgery for lung cancer were stimulated with TNF-α (50 ng/mL), IL-1α (5 ng/mL), added alone or in combination, and TGF-β1 (5 ng/mL). After treatment with niclosamide at 30 nM and 100 nM concentrations, expression of collagen type I, collagen type III, and fibronectin was studied by total RNA isolation and qRT-PCR and protein collagen secretion with the use of Sircol collagen assay. The migration of SELMs was assessed by a wound-healing assay. Niclosamide had no effect on baseline SELM fibrotic factor expression. When stimulated with TGF-β1, IL-1α, and/or TNF-α, SELM expression of collagen type I, type III, and fibronectin were upregulated, as was the secretion of total collagen in the culture medium. Treatment with niclosamide attenuated the effects of cytokine stimulation leading to a notable decrease in the mRNA expression of collagen type I, type III, and fibronectin in a concentration-dependent manner. SELM collagen secretion was also reduced by niclosamide at 100 nM concentration when examined at the protein level. Migration of both TGF-β1 stimulated and unstimulated SELMs was also inhibited by niclosamide. In this study, we highlight the anti-fibrotic properties of niclosamide on SELMs under stimulation with pro-fibrotic and pro-inflammatory cytokines, thus proposing this compound as a possible new therapeutic agent against lung fibrosis. Full article
(This article belongs to the Special Issue Treatment for Pulmonary Fibrosis, Volume II)
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18 pages, 6288 KiB  
Article
Two-Pore-Domain Potassium Channel TREK–1 Mediates Pulmonary Fibrosis through Macrophage M2 Polarization and by Direct Promotion of Fibroblast Differentiation
by Yunna Zhang, Jiafeng Fu, Yang Han, Dandan Feng, Shaojie Yue, Yan Zhou and Ziqiang Luo
Biomedicines 2023, 11(5), 1279; https://doi.org/10.3390/biomedicines11051279 - 26 Apr 2023
Cited by 2 | Viewed by 2041
Abstract
Idiopathic pulmonary fibrosis (IPF) is a devastating disease characterized by myofibroblast proliferation and abnormal accumulation of extracellular matrix in the lungs. After lung injury, M2 macrophages mediate the pathogenesis of pulmonary fibrosis by secreting fibrotic cytokines that promote myofibroblast activation. The TWIK-related potassium [...] Read more.
Idiopathic pulmonary fibrosis (IPF) is a devastating disease characterized by myofibroblast proliferation and abnormal accumulation of extracellular matrix in the lungs. After lung injury, M2 macrophages mediate the pathogenesis of pulmonary fibrosis by secreting fibrotic cytokines that promote myofibroblast activation. The TWIK-related potassium channel (TREK–1, also known as KCNK2) is a K2P channel that is highly expressed in cardiac, lung, and other tissues; it worsens various tumors, such as ovarian cancer and prostate cancer, and mediates cardiac fibrosis. However, the role of TREK–1 in lung fibrosis remains unclear. This study aimed to examine the effects of TREK–1 on bleomycin (BLM)-induced lung fibrosis. The results show that TREK–1 knockdown, mediated by the adenovirus or pharmacological inhibition of TREK–1 with fluoxetine, resulted in diminished BLM-induced lung fibrosis. TREK–1 overexpression in macrophages remarkably increased the M2 phenotype, resulting in fibroblast activation. Furthermore, TREK–1 knockdown and fluoxetine administration directly reduced the differentiation of fibroblasts to myofibroblasts by inhibiting the focal adhesion kinase (FAK)/p38 mitogen-activated protein kinases (p38)/Yes-associated protein (YAP) signaling pathway. In conclusion, TREK–1 plays a central role in the pathogenesis of BLM-induced lung fibrosis, which serves as a theoretical basis for the inhibition of TREK–1 as a potential therapy protocol for lung fibrosis. Full article
(This article belongs to the Special Issue Treatment for Pulmonary Fibrosis, Volume II)
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Review

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15 pages, 691 KiB  
Review
HSP47: A Therapeutic Target in Pulmonary Fibrosis
by Noriho Sakamoto, Daisuke Okuno, Takatomo Tokito, Hirokazu Yura, Takashi Kido, Hiroshi Ishimoto, Yoshimasa Tanaka and Hiroshi Mukae
Biomedicines 2023, 11(9), 2387; https://doi.org/10.3390/biomedicines11092387 - 25 Aug 2023
Cited by 3 | Viewed by 1651
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by a progressive decline in lung function and poor prognosis. The deposition of the extracellular matrix (ECM) by myofibroblasts contributes to the stiffening of lung tissue and impaired oxygen exchange in IPF. Type [...] Read more.
Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by a progressive decline in lung function and poor prognosis. The deposition of the extracellular matrix (ECM) by myofibroblasts contributes to the stiffening of lung tissue and impaired oxygen exchange in IPF. Type I collagen is the major ECM component and predominant collagen protein deposited in chronic fibrosis, suggesting that type I collagen could be a target of drugs for fibrosis treatment. Heat shock protein 47 (HSP47), encoded by the serpin peptidase inhibitor clade H, member 1 gene, is a stress-inducible collagen-binding protein. It is an endoplasmic reticulum-resident molecular chaperone essential for the correct folding of procollagen. HSP47 expression is increased in cellular and animal models of pulmonary fibrosis and correlates with pathological manifestations in human interstitial lung diseases. Various factors affect HSP47 expression directly or indirectly in pulmonary fibrosis models. Overall, understanding the relationship between HSP47 expression and pulmonary fibrosis may contribute to the development of novel therapeutic strategies. Full article
(This article belongs to the Special Issue Treatment for Pulmonary Fibrosis, Volume II)
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17 pages, 1562 KiB  
Review
Epigenetics Approaches toward Precision Medicine for Idiopathic Pulmonary Fibrosis: Focus on DNA Methylation
by Wiwin Is Effendi and Tatsuya Nagano
Biomedicines 2023, 11(4), 1047; https://doi.org/10.3390/biomedicines11041047 - 28 Mar 2023
Cited by 3 | Viewed by 2282
Abstract
Genetic information is not transmitted solely by DNA but by the epigenetics process. Epigenetics describes molecular missing link pathways that could bridge the gap between the genetic background and environmental risk factors that contribute to the pathogenesis of pulmonary fibrosis. Specific epigenetic patterns, [...] Read more.
Genetic information is not transmitted solely by DNA but by the epigenetics process. Epigenetics describes molecular missing link pathways that could bridge the gap between the genetic background and environmental risk factors that contribute to the pathogenesis of pulmonary fibrosis. Specific epigenetic patterns, especially DNA methylation, histone modifications, long non-coding, and microRNA (miRNAs), affect the endophenotypes underlying the development of idiopathic pulmonary fibrosis (IPF). Among all the epigenetic marks, DNA methylation modifications have been the most widely studied in IPF. This review summarizes the current knowledge concerning DNA methylation changes in pulmonary fibrosis and demonstrates a promising novel epigenetics-based precision medicine. Full article
(This article belongs to the Special Issue Treatment for Pulmonary Fibrosis, Volume II)
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