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Advances in Lung Inflammation, Injury, and Repair (Second Edition)

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: 30 September 2025 | Viewed by 405

Special Issue Editor


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Guest Editor
Department of Pediatrics, Universiy of California Los Angeles, Los Angeles, CA 90095, USA
Interests: acute lung injury; acute respiratory distress syndrome; lung; inflammation; respiratory failure; hyperoxia; mechanical ventilation; cytokines; ion channels; potassium; calcium
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This is a continued series on the hot topic of “Advances in Lung Inflammation, Injury, and Repair”. Our first Special Issue on this topic received interesting contributions and discussions, which may be viewed through the following link: https://www.mdpi.com/journal/ijms/special_issues/Lung_Research.

Lung inflammation, injury, and repair are pathophysiological processes shared by multiple pulmonary disease entities. Most recently, the COVID-19 pandemic highlighted the catastrophic consequences associated with the dysregulation of these processes and our limited understanding of the underlying molecular mechanisms, which is reflected in the limited therapeutic armamentarium currently available for our patients. In many cases, these pathophysiological findings are grouped together as acute respiratory distress syndrome (ARDS), but a substantial number of patients suffering from similarly dysregulated lung inflammation, injury, and repair mechanisms are not meeting ARDS criteria and yet are still at high risk for poor outcomes and short- and long-term morbidity and mortality.

To address these challenges, within the IJMS section of “Molecular Pathology, Diagnostics, and Therapeutics”, we are proposing a Special Issue titled “Advances in Lung Inflammation, Injury, and Repair (Second Edition)” to create a state-of-the-art work product summarizing our current understanding and knowledge gaps in this field and propose future approaches, novel targets, and next-generation experimental models. Since lung injury can be triggered by a variety of insults, including (but not limited to) viral and bacterial infections, sepsis, trauma, blood transfusion, gastric content aspiration, cardiopulmonary resuscitation, toxic inhalations, medications, and autoimmune processes, this interdisciplinary collection of manuscripts aims to provide a comprehensive resource on molecular pathology, diagnostics, and therapeutics in the fields of lung inflammation, injury, and repair for a large audience, including research and medical trainees, pulmonary physiologists and pathologists, general practitioners and pulmonary/critical care specialists, nurses, and respiratory therapists.

Dr. Andreas Schwingshackl
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
  • inflammation
  • injury
  • repair
  • fibrosis
  • diagnostics
  • therapeutics
  • acute respiratory distress syndrome

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Published Papers (1 paper)

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Research

19 pages, 3253 KiB  
Article
The SGLT2 Inhibitor Empagliflozin Mitigates the Harmful Effects of Methylglyoxal Exposure on Ovalbumin-Induced Mouse Airway Inflammation
by Matheus L. Medeiros, Akila L. Oliveira and Edson Antunes
Int. J. Mol. Sci. 2025, 26(12), 5753; https://doi.org/10.3390/ijms26125753 - 16 Jun 2025
Viewed by 323
Abstract
Asthma is a chronic inflammatory airway disease that can be aggravated by metabolic comorbidities such as type 2 diabetes mellitus (DM2) and obesity. Elevated levels of methylglyoxal (MGO), a reactive glycolysis byproduct, have been associated with exacerbation of allergic airway disease. SGLT2 inhibitors [...] Read more.
Asthma is a chronic inflammatory airway disease that can be aggravated by metabolic comorbidities such as type 2 diabetes mellitus (DM2) and obesity. Elevated levels of methylglyoxal (MGO), a reactive glycolysis byproduct, have been associated with exacerbation of allergic airway disease. SGLT2 inhibitors have been successfully employed in DM2 treatment. Here, we hypothesized that elimination of MGO might be a potential anti-inflammatory mechanism of SGLT2 inhibitors. This study aimed to evaluate the effects of empagliflozin on ovalbumin (OVA)-induced airway inflammation in mice chronically exposed to MGO. Male C57BL/6 mice sensitized with OVA were exposed to 0.5% MGO for 12 weeks and treated with empagliflozin (10 mg/kg, gavage, two weeks). MGO exposure significantly enhanced airway eosinophil infiltration, mucus production and collagen deposition, as well as levels of IL-4, IL-5, eotaxin and TNF-α. Empagliflozin treatment significantly reduced OVA-induced airway disease, which was accompanied by reductions in IgE, IL-4, IL-5, eotaxin, and TNF-α levels. Empagliflozin significantly reduced the MGO levels in serum, and immunohistochemical staining, and protein expression of MGO-hydroimidazolone (MG-H1), while increasing IL-10 levels and glyoxylase-1 (GLO 1) activity in lungs. In conclusion, empagliflozin efficiently removes MGO from circulation, while increasing the MGO detoxification by GLO 1, thereby mitigating the OVA-induced inflammation in MGO-exposed mice. Full article
(This article belongs to the Special Issue Advances in Lung Inflammation, Injury, and Repair (Second Edition))
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