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Lung Diseases Molecular Pathogenesis and Therapy
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Lung Diseases Molecular Pathogenesis and Therapy

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 July 2025) | Viewed by 8183

Special Issue Editor

Dr. Kazufumi Nakamura

E-Mail Website
Guest Editor
Center for Advanced Heart Failure, Okayama University Hospital, Okayama, Japan
Interests: cardiovascular system; cardiac sarcoidosis; coronary artery disease; vein anastomosis; dilated cardiomyopathy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The most common cause of cancer death worldwide is lung cancer, but other respiratory pathologies also cause high mortality, such as chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, infections such as influenza and SARS-CoV-2, acute respiratory distress syndrome (ARDS), pulmonary hypertension, and asthma. The 5-year survival rate remains very low for patients with advanced stage lung cancer. Many drugs have already been proposed for the treatment of lung diseases. Few of them are in clinical trials and have the potential to cure infectious diseases.

The aim of this Special Issue is to provide a platform for the mechanistic investigation of the molecular pathogenesis of lung diseases, with a special focus on potential drug therapies. We warmly welcome the submission of original articles and outcome-based reviews from molecular viewpoints.

Dr. Kazufumi Nakamura
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • lung diseases
  • drug therapy
  • chronic obstructive pulmonary disease
  • lung cancer
  • lung fibrosis
  • pulmonary hypertension
  • asthma

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Published Papers (5 papers)

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Research

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16 pages, 1961 KiB  
Article
PAI-1 Inhibitor TM5441 Attenuates Emphysema and Airway Inflammation in a Murine Model of Chronic Obstructive Pulmonary Disease
by Kyohei Oishi, Hideki Yasui, Yusuke Inoue, Hironao Hozumi, Yuzo Suzuki, Masato Karayama, Kazuki Furuhashi, Noriyuki Enomoto, Tomoyuki Fujisawa, Takahiro Horinouchi, Takayuki Iwaki, Yuko Suzuki, Toshio Miyata, Naoki Inui and Takafumi Suda
Int. J. Mol. Sci. 2025, 26(15), 7086; https://doi.org/10.3390/ijms26157086 - 23 Jul 2025
Viewed by 125
Abstract
Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide, primarily driven by chronic airway inflammation due to cigarette smoke exposure. Despite its burden, however, current anti-inflammatory therapies offer limited efficacy in preventing disease progression. Plasminogen activator inhibitor-1 (PAI-1), [...] Read more.
Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide, primarily driven by chronic airway inflammation due to cigarette smoke exposure. Despite its burden, however, current anti-inflammatory therapies offer limited efficacy in preventing disease progression. Plasminogen activator inhibitor-1 (PAI-1), as a key regulator of fibrinolysis, has recently been implicated in structural airway changes and persistent inflammation in patients with COPD. This study aimed to investigate the ability of the PAI-1 inhibitor TM5441 to attenuate airway inflammation and structural lung damage induced by a cigarette smoke extract (CSE) in a mouse model. Mice received intratracheal CSE or vehicle on days 1, 8, and 15, and were sacrificed on day 22. TM5441 (20 mg/kg) was administered orally from days 1 to 22. The CSE significantly increased the mean linear intercept, destructive index, airway resistance, and reductions in dynamic compliance. The CSE also increased the numbers of neutrophils and macrophages in the bronchoalveolar lavage fluid, systemic PAI-1 activity, and neutrophil elastase mRNA and protein expression in the lungs. TM5441 treatment significantly suppressed these changes without affecting coagulation time. These findings suggest that TM5441 may be a novel therapeutic agent for COPD by targeting PAI-1-mediated airway inflammation and emphysema. Full article
(This article belongs to the Special Issue Lung Diseases Molecular Pathogenesis and Therapy)
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13 pages, 1390 KiB  
Article
Twelve-Month CPAP Therapy Modulates BDNF Levels in Patients with Severe Obstructive Sleep Apnea: Implications for Metabolic and Treatment Compliance
by Urszula Karwowska, Aleksandra Kudrycka, Karol Pierzchała, Robert Stawski, Hanna Jerczyńska, Piotr Białasiewicz and Wojciech Kuczyński
Int. J. Mol. Sci. 2025, 26(12), 5855; https://doi.org/10.3390/ijms26125855 - 18 Jun 2025
Viewed by 540
Abstract
Brain-derived neurotrophic factor (BDNF) is a neurotrophin involved in the regulation of synaptic plasticity and metabolic processes, including glucose metabolism and insulin sensitivity. In patients with obstructive sleep apnea (OSA), recurrent episodes of intermittent hypoxia may stimulate BDNF expression as a compensatory neuroprotective [...] Read more.
Brain-derived neurotrophic factor (BDNF) is a neurotrophin involved in the regulation of synaptic plasticity and metabolic processes, including glucose metabolism and insulin sensitivity. In patients with obstructive sleep apnea (OSA), recurrent episodes of intermittent hypoxia may stimulate BDNF expression as a compensatory neuroprotective response. OSA is associated with metabolic disturbances, such as increased insulin resistance and a higher risk of type 2 diabetes. Continuous positive airway pressure (CPAP) therapy may influence both BDNF levels and metabolic outcomes. The aim of this study was to evaluate changes in BDNF concentration and glucose metabolism in patients with OSA, with particular emphasis on the effect of long-term CPAP therapy. Sixty-six adult patients with OSA confirmed by polysomnography were enrolled and divided into severe (s-OSA) and non-severe (ns-OSA) groups. Fasting blood samples were collected to measure glucose, insulin, and BDNF concentrations. Patients with s-OSA were re-evaluated after 12 months of CPAP therapy and further classified as compliant (sc-OSA) or non-compliant (snc-OSA) based on recorded device usage. The same biochemical parameters were assessed after the 12-month follow-up. Baseline BDNF levels were significantly higher in the s-OSA group compared to the ns-OSA group (20.1 ng/mL vs. 8.1 ng/mL, p = 0.02) and correlated with the apnea–hypopnea index (AHI, r = 0.38, p = 0.02). In the nsc-OSA group, BDNF concentrations increased significantly after 12 months (16.2 ng/mL vs. 35.5 ng/mL, p < 0.001), while no significant change was observed in the sc-OSA group (24.4 ng/mL vs. 27.4 ng/mL, p = 0.33). Among sc-OSA patients, a significant improvement in insulin resistance was noted, although no significant changes were observed in fasting glucose or insulin levels. Increased BDNF levels were observed in patients with s-OSA compared to ns-OSA. Compliant CPAP therapy was associated with reduced insulin resistance and no further BDNF increase, in contrast to non-compliance, suggesting a beneficial effect of CPAP on glucose metabolism and BDNF regulation. These findings support the hypothesis that both neurotrophic and metabolic responses in OSA may be modulated by disease severity and therapy adherence. Full article
(This article belongs to the Special Issue Lung Diseases Molecular Pathogenesis and Therapy)
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11 pages, 3234 KiB  
Article
SGLT2 Inhibitors Empagliflozin and Canagliflozin Ameliorate Allergic Asthma Responses in Mice
by Ye-Eul Lee and Dong-Soon Im
Int. J. Mol. Sci. 2024, 25(14), 7567; https://doi.org/10.3390/ijms25147567 - 10 Jul 2024
Cited by 6 | Viewed by 2086
Abstract
Inhibitors of sodium/glucose cotransporter 2 (SGLT2), such as empagliflozin and canagliflozin, have been widely used to block glucose reabsorption in the proximal tubules of kidneys in patients with diabetes. A meta-analysis suggested that SGLT2 inhibitors are associated with a decreased risk of asthma [...] Read more.
Inhibitors of sodium/glucose cotransporter 2 (SGLT2), such as empagliflozin and canagliflozin, have been widely used to block glucose reabsorption in the proximal tubules of kidneys in patients with diabetes. A meta-analysis suggested that SGLT2 inhibitors are associated with a decreased risk of asthma development. Therefore, we investigated whether SGLT2 inhibitors could suppress allergic asthma. Empagliflozin and canagliflozin suppressed the in vitro degranulation reaction induced by antigens in a concentration-dependent manner in RBL-2H3 mast cells. Empagliflozin and canagliflozin were administered to BALB/c mice sensitized to ovalbumin (OVA). The administration of empagliflozin or canagliflozin significantly suppressed OVA-induced airway hyper-responsiveness and increased the number of immune cells and pro-inflammatory cytokine mRNA expression levels in bronchoalveolar lavage fluid. The administration of empagliflozin and canagliflozin also suppressed OVA-induced histopathological changes in the lungs. Empagliflozin and canagliflozin also suppressed serum IgE levels. These results suggested that empagliflozin and canagliflozin may be applicable for the treatment of allergic asthma by suppressing immune responses. Full article
(This article belongs to the Special Issue Lung Diseases Molecular Pathogenesis and Therapy)
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Review

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12 pages, 1147 KiB  
Review
Role of Regulatory T Cells in Pulmonary Ageing and COPD Development
by Virginija Šileikienė and Laimutė Jurgauskienė
Int. J. Mol. Sci. 2025, 26(8), 3721; https://doi.org/10.3390/ijms26083721 - 15 Apr 2025
Viewed by 965
Abstract
Chronic obstructive pulmonary disease (COPD) is recognized as a long-term inflammatory lung condition, predominantly resulting from smoking tobacco. While all smokers exhibit some level of pulmonary inflammation, only about 15–20% go on to develop significant COPD, indicating that specific individual factors may enhance [...] Read more.
Chronic obstructive pulmonary disease (COPD) is recognized as a long-term inflammatory lung condition, predominantly resulting from smoking tobacco. While all smokers exhibit some level of pulmonary inflammation, only about 15–20% go on to develop significant COPD, indicating that specific individual factors may enhance these inflammatory responses and contribute to the disease’s progression. T regulatory cell (Treg) activity is crucial in mediating pulmonary inflammation in COPD. With accumulating evidence supporting the autoimmune characteristics of COPD, there has been an increasing focus on the role Treg cells play in the disease’s initiation and development. This article aims to review the existing literature regarding Treg cells and their influence on COPD pathogenesis and lung ageing. Treg-mediated suppression is a critical mechanism in the negative regulation of immune-related inflammation, which is significant in various disorders, including autoimmunity, allergies, infections (both acute and chronic), and cancer. The lungs of ageing individuals often resemble those affected by COPD, leading to the perception of COPD as a condition that accelerates lung ageing. Changes in Treg cells with age correspond to decreased adaptive immune responses and a higher likelihood of immune-related disorders. The increased presence of Treg cells in older adults may help explain several immunological conditions commonly associated with ageing, which include malignancies, infections, and COPD. Full article
(This article belongs to the Special Issue Lung Diseases Molecular Pathogenesis and Therapy)
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22 pages, 1547 KiB  
Review
Pathophysiology of Group 3 Pulmonary Hypertension Associated with Lung Diseases and/or Hypoxia
by Kazufumi Nakamura, Satoshi Akagi, Kentaro Ejiri, Satoshi Taya, Yukihiro Saito, Kazuhiro Kuroda, Yoichi Takaya, Norihisa Toh, Rie Nakayama, Yuki Katanosaka and Shinsuke Yuasa
Int. J. Mol. Sci. 2025, 26(2), 835; https://doi.org/10.3390/ijms26020835 - 20 Jan 2025
Cited by 2 | Viewed by 3757
Abstract
Pulmonary hypertension associated with lung diseases and/or hypoxia is classified as group 3 in the clinical classification of pulmonary hypertension. The efficacy of existing selective pulmonary vasodilators for group 3 pulmonary hypertension is still unknown, and it is currently associated with a poor [...] Read more.
Pulmonary hypertension associated with lung diseases and/or hypoxia is classified as group 3 in the clinical classification of pulmonary hypertension. The efficacy of existing selective pulmonary vasodilators for group 3 pulmonary hypertension is still unknown, and it is currently associated with a poor prognosis. The mechanisms by which pulmonary hypertension occurs include hypoxic pulmonary vasoconstriction, pulmonary vascular remodeling, a decrease in pulmonary vascular beds, endothelial dysfunction, endothelial-to-mesenchymal transition, mitochondrial dysfunction, oxidative stress, hypoxia-inducible factors (HIFs), inflammation, microRNA, and genetic predisposition. Among these, hypoxic pulmonary vasoconstriction and subsequent pulmonary vascular remodeling are characteristic factors involving the pulmonary vasculature and are the focus of this review. Several factors have been reported to mediate vascular remodeling induced by hypoxic pulmonary vasoconstriction, such as HIF-1α and mechanosensors, including TRP channels. New therapies that target novel molecules, such as mechanoreceptors, to inhibit vascular remodeling are awaited. Full article
(This article belongs to the Special Issue Lung Diseases Molecular Pathogenesis and Therapy)
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