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New Perspective in the Molecular Pathways Involved in Acute and Chronic Lung Injury

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: 20 June 2025 | Viewed by 7754

Special Issue Editor

Dr. Marika Cordaro

E-Mail Website
Guest Editor
Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, 98125 Messina, Italy
Interests: oxidative stress; nutrition; cell physiology; animal model; inflammation; molecular pathways
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) describe clinical syndromes of acute respiratory failure with substantial morbidity and mortality. Even in patients who survive ALI, there is evidence that their long-term quality of life is adversely affected. Recent advances have been made in the understanding of the epidemiology, pathogenesis, and treatment of this disease. However, more progress is needed to further reduce mortality and morbidity from ALI and ARDS. Because this syndrome of acute respiratory failure is so common both in the United States and worldwide, it is fair to say that ALI/ARDS is an unmet medical need. In other words, novel therapies need to be developed to further improve clinical outcomes. This Special Issue aims to provide an overview of the current and future definitions, pathogenesis, and treatment of acute lung injury. Original articles/reviews on natural or synthetic compounds as new treatments for respiratory disease and on the effects of environmental pollutants (such as endocrine disruption) that explore the molecular pathways involved during ALI/ARDS are welcome.

Dr. Marika Cordaro
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

  • acute lung injury
  • chronic lung injury
  • molecular pathways
  • treatment
  • therapeutic targets
  • inflammation
  • oxidative stress
  • respiratory disease

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Published Papers (5 papers)

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Research

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20 pages, 7778 KiB  
Article
Claudin-17 Deficiency Drives Vascular Permeability and Inflammation Causing Lung Injury
by Mir S. Adil, Varun Parvathagiri, Abdulaziz H. Alanazi, Daulat Khulood, S. Priya Narayanan and Payaningal R. Somanath
Int. J. Mol. Sci. 2025, 26(8), 3612; https://doi.org/10.3390/ijms26083612 - 11 Apr 2025
Viewed by 216
Abstract
The role of claudin-17 (Cldn17), a tight-junction protein, in vascular permeability remains unclear. We investigated the impact of Cldn17 suppression on vascular permeability. The Miles assay demonstrated significantly increased vascular permeability in the lungs and skin of Cldn17−/− mice, as evidenced by [...] Read more.
The role of claudin-17 (Cldn17), a tight-junction protein, in vascular permeability remains unclear. We investigated the impact of Cldn17 suppression on vascular permeability. The Miles assay demonstrated significantly increased vascular permeability in the lungs and skin of Cldn17−/− mice, as evidenced by elevated Evan’s blue dye extravasation. The Matrigel plug assay demonstrated increased hemoglobin extravasation. Histopathological analysis revealed alveolar flooding, inflammatory cell infiltration, and lung injury in Cldn17−/− lungs. Wet/dry lung weight ratios indicated pulmonary edema, supporting the role of Cldn17 in pulmonary fluid balance, which was exacerbated with lipopolysaccharide administration. Ribosomal nucleic acid sequencing identified distinct transcriptional changes, with the principal component analysis showing clear clustering. Differential gene expression analysis highlighted significant alterations in inflammatory and metabolic pathways. Gene ontology and pathway enrichment analyses revealed the upregulation of immune-related processes, including leukocyte adhesion, interferon–gamma response, and neutrophil degranulation, alongside metabolic dysregulation affecting lipid transport and cytoskeletal organization. Reactome pathway analysis implicated Cldn17 in antigen presentation, interleukin-17 signaling, and inflammatory responses. These findings establish Cldn17 as a critical regulator of vascular permeability and immune homeostasis. Its deficiency drives vascular leakage, exacerbates lung injury, and alters immune signaling pathways, underscoring its potential as a therapeutic target for inflammatory lung diseases. Full article
(This article belongs to the Special Issue New Perspective in the Molecular Pathways Involved in Acute and Chronic Lung Injury)
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13 pages, 4955 KiB  
Article
Pirfenidone Alleviates Inflammation and Fibrosis of Acute Respiratory Distress Syndrome by Modulating the Transforming Growth Factor-β/Smad Signaling Pathway
by Seung Sook Paik, Jeong Mi Lee, Il-Gyu Ko, Sae Rom Kim, Sung Wook Kang, Jin An, Jin Ah Kim, Dongyon Kim, Lakkyong Hwang, Jun-Jang Jin, Sang-Hoon Kim, Jun-Youl Cha and Cheon Woong Choi
Int. J. Mol. Sci. 2024, 25(15), 8014; https://doi.org/10.3390/ijms25158014 - 23 Jul 2024
Cited by 1 | Viewed by 1764
Abstract
Acute respiratory distress syndrome (ARDS) occurs as an acute onset condition, and patients present with diffuse alveolar damage, refractory hypoxemia, and non-cardiac pulmonary edema. ARDS progresses through an initial exudative phase, an inflammatory phase, and a final fibrotic phase. Pirfenidone, a powerful anti-fibrotic [...] Read more.
Acute respiratory distress syndrome (ARDS) occurs as an acute onset condition, and patients present with diffuse alveolar damage, refractory hypoxemia, and non-cardiac pulmonary edema. ARDS progresses through an initial exudative phase, an inflammatory phase, and a final fibrotic phase. Pirfenidone, a powerful anti-fibrotic agent, is known as an agent that inhibits the progression of fibrosis in idiopathic pulmonary fibrosis. In this study, we studied the treatment efficiency of pirfenidone on lipopolysaccharide (LPS) and bleomycin-induced ARDS using rats. The ARDS rat model was created by the intratracheal administration of 3 mg/kg LPS of and 3 mg/kg of bleomycin dissolved in 0.2 mL of normal saline. The pirfenidone treatment group was administered 100 or 200 mg/kg of pirfenidone dissolved in 0.5 mL distilled water orally 10 times every 2 days for 20 days. The administration of LPS and bleomycin intratracheally increased lung injury scores and significantly produced pro-inflammatory cytokines. ARDS induction increased the expressions of transforming growth factor (TGF)-β1/Smad-2 signaling factors. Additionally, matrix metalloproteinase (MMP)-9/tissue inhibitor of metalloproteinase (TIMP)-1 imbalance occurred, resulting in enhanced fibrosis-related factors. Treatment with pirfenidone strongly suppressed the expressions of TGF-β1/Smad-2 signaling factors and improved the imbalance of MMP-9/TIMP-1 compared to the untreated group. These effects led to a decrease in fibrosis factors and pro-inflammatory cytokines, promoting the recovery of damaged lung tissue. These results of this study showed that pirfenidone administration suppressed inflammation and fibrosis in the ARDS animal model. Therefore, pirfenidone can be considered a new early treatment for ARDS. Full article
(This article belongs to the Special Issue New Perspective in the Molecular Pathways Involved in Acute and Chronic Lung Injury)
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23 pages, 2060 KiB  
Article
Dual Exposure to E-Cigarette Vapour and Cigarette Smoke Results in Poorer Airway Cell, Monocyte, and Macrophage Function Than Single Exposure
by Rhys Hamon, Leigh Thredgold, Asiri Wijenayaka, Nicole Anne Bastian and Miranda P. Ween
Int. J. Mol. Sci. 2024, 25(11), 6071; https://doi.org/10.3390/ijms25116071 - 31 May 2024
Cited by 2 | Viewed by 1792
Abstract
E-cigarette users predominantly also continue to smoke cigarettes. These Dual Users either consume e-cigarettes in locations where smoking is not allowed, but vaping is, or to reduce their consumption of cigarettes, believing it will lead to harm reduction. Whilst it is known that [...] Read more.
E-cigarette users predominantly also continue to smoke cigarettes. These Dual Users either consume e-cigarettes in locations where smoking is not allowed, but vaping is, or to reduce their consumption of cigarettes, believing it will lead to harm reduction. Whilst it is known that e-cigarette vapour is chemically less complex than cigarette smoke, it has a distinct chemical profile, and very little is known about the health impacts of exposure to both chemical profiles vs. either alone. We simultaneously exposed cells in vitro to non-toxic levels of e-cigarette vapour extract (EVE) and cigarette smoke extract (CSE) to determine their effects on 16HBE14o- airway epithelial cell metabolism and inflammatory response, as well as immune cell (THP-1 cells and monocyte-derived macrophages (MDM) from healthy volunteers) migration, phagocytosis, and inflammatory response. We observed increased toxicity, reduced metabolism (a marker of proliferation) in airway epithelial cells, and reduced monocyte migration, macrophage phagocytosis, and altered chemokine production after exposure to either CSE or EVE. These cellular responses were greater after dual exposure to CSE and EVE. The airway epithelial cells from smokers showed reduced metabolism after EVE (the Switcher model) and dual CSE and EVE exposure. When EVE and CSE were allowed to interact, the chemicals were found to be altered, and new chemicals were also found compared to the CSE and EVE profiles. Dual exposure to e-cigarette vapour and cigarette smoke led to worse functional outcomes in cells compared to either single exposure alone, adding to limited data that dual use may be more dangerous than smoking only. Full article
(This article belongs to the Special Issue New Perspective in the Molecular Pathways Involved in Acute and Chronic Lung Injury)
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15 pages, 9713 KiB  
Article
Inhibition of Fatty Acid Amide Hydrolase (FAAH) Regulates NF-kb Pathways Reducing Bleomycin-Induced Chronic Lung Inflammation and Pulmonary Fibrosis
by Tiziana Genovese, Andrea Duranti, Francesco Monaco, Rosalba Siracusa, Roberta Fusco, Daniela Impellizzeri, Ramona D’Amico, Marika Cordaro, Salvatore Cuzzocrea and Rosanna Di Paola
Int. J. Mol. Sci. 2023, 24(12), 10125; https://doi.org/10.3390/ijms241210125 - 14 Jun 2023
Cited by 3 | Viewed by 2113
Abstract
The deadly interstitial lung condition known as idiopathic pulmonary fibrosis (IPF) worsens over time and for no apparent reason. The traditional therapy approaches for IPF, which include corticosteroids and immunomodulatory drugs, are often ineffective and can have noticeable side effects. The endocannabinoids are [...] Read more.
The deadly interstitial lung condition known as idiopathic pulmonary fibrosis (IPF) worsens over time and for no apparent reason. The traditional therapy approaches for IPF, which include corticosteroids and immunomodulatory drugs, are often ineffective and can have noticeable side effects. The endocannabinoids are hydrolyzed by a membrane protein called fatty acid amide hydrolase (FAAH). Increasing endogenous levels of endocannabinoid by pharmacologically inhibiting FAAH results in numerous analgesic advantages in a variety of experimental models for pre-clinical pain and inflammation. In our study, we mimicked IPF by administering intratracheal bleomycin, and we administered oral URB878 at a dose of 5 mg/kg. The histological changes, cell infiltration, pro-inflammatory cytokine production, inflammation, and nitrosative stress caused by bleomycin were all reduced by URB878. Our data clearly demonstrate for the first time that the inhibition of FAAH activity was able to counteract not only the histological alteration bleomycin-induced but also the cascade of related inflammatory events. Full article
(This article belongs to the Special Issue New Perspective in the Molecular Pathways Involved in Acute and Chronic Lung Injury)
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Review

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29 pages, 1282 KiB  
Review
N-Acetylcysteine in the Treatment of Acute Lung Injury: Perspectives and Limitations
by Daniela Mokra, Igor Porvaznik and Juraj Mokry
Int. J. Mol. Sci. 2025, 26(6), 2657; https://doi.org/10.3390/ijms26062657 - 15 Mar 2025
Viewed by 1107
Abstract
N-acetylcysteine (NAC) can take part in the treatment of chronic respiratory diseases because of the potent mucolytic, antioxidant, and anti-inflammatory effects of NAC. However, less is known about its use in the treatment of acute lung injury. Nowadays, an increasing number of studies [...] Read more.
N-acetylcysteine (NAC) can take part in the treatment of chronic respiratory diseases because of the potent mucolytic, antioxidant, and anti-inflammatory effects of NAC. However, less is known about its use in the treatment of acute lung injury. Nowadays, an increasing number of studies indicates that early administration of NAC may reduce markers of oxidative stress and alleviate inflammation in animal models of acute lung injury (ALI) and in patients suffering from distinct forms of acute respiratory distress syndrome (ARDS) or pulmonary infections including community-acquired pneumonia or Coronavirus Disease (COVID)-19. Besides low costs, easy accessibility, low toxicity, and rare side effects, NAC can also be combined with other drugs. This article provides a review of knowledge on the mechanisms of inflammation and oxidative stress in various forms of ALI/ARDS and critically discusses experience with the use of NAC in these disorders. For preparing the review, articles published in the English language from the PubMed database were used. Full article
(This article belongs to the Special Issue New Perspective in the Molecular Pathways Involved in Acute and Chronic Lung Injury)
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