Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
Cellular and Molecular Mechanisms of Acute Lung Injury
ijms-logo
Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Cellular and Molecular Mechanisms of Acute 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 August 2025 | Viewed by 2613

Special Issue Editor

Dr. Ahilanandan Dushianthan

E-Mail Website
Guest Editor
Perioperative and Critical Care Theme, NIHR Southampton Biomedical Research Centre, University Hospital Southampton NHS Foundation Trust, Southampton SO16 6YD, Hampshire, UK
Interests: lung injury; ARDS; mechanical ventilation; ICU; non-invasive ventilation; oxygen
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Acute lung injury imposes a substantial health and economic burden worldwide. Lung infection and the subsequent host immune response can lead to alveolar epithelial and endothelial injury, impairing gas exchange and necessitating hospitalisation for oxygen therapy. Despite significant advances in knowledge, acute lung injury or acute respiratory distress syndrome (ARDS) remains a heterogeneous disease process, and management is limited due to a lack of therapeutic targets. The endophenotypes and underlying molecular mechanisms vary among patients, leading to differences in treatment response and outcomes. The complex interplay of multiple cellular and molecular mechanisms, including neutrophil-mediated immune response, alveolar epithelial injury and apoptosis, surfactant dysfunction, alterations in alveolar glycocalyx and extracellular matrix, microvascular damage/thrombosis and increased vascular permeability, results in florid non-cardiogenic pulmonary oedema and poor lung compliance. In addition, treatments such as oxygen therapy, intravenous fluid therapy/balance, transfusion of blood products and initiation of invasive or non-invasive mechanical ventilation can contribute to or exacerbate the existing lung injury. In this Special Issue, we aim to explore the molecular mechanisms that are important in the development and resolution of acute lung injury which may offer insights into future therapeutic targets.

Dr. Ahilanandan Dushianthan
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
  • lung infection
  • acute respiratory distress syndrom
  • neutrophil-mediated immune response
  • alveolar epithelial injury
  • pulmonary oedema

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

18 pages, 3307 KiB  
Article
Razuprotafib Does Not Improve Microcirculatory Perfusion Disturbances nor Renal Edema in Rats on Extracorporeal Circulation
by Dionne P. C. Dubelaar, Carolien Volleman, Philippa G. Phelp, Roselique Ibelings, Iris Voorn, Anita M. Tuip-de Boer, Chantal A. Polet, Joris J. Roelofs, Alexander P. J. Vlaar, Matijs van Meurs and Charissa E. van den Brom
Int. J. Mol. Sci. 2025, 26(7), 3000; https://doi.org/10.3390/ijms26073000 - 25 Mar 2025
Viewed by 303
Abstract
Extracorporeal membrane oxygenation (ECMO) can be a life-saving intervention, but it is associated with high complication rates. ECMO induces systemic inflammation and endothelial hyperpermeability, thereby causing tissue edema, microcirculatory perfusion disturbances, and organ failure. This study investigated whether the inhibition of vascular endothelial [...] Read more.
Extracorporeal membrane oxygenation (ECMO) can be a life-saving intervention, but it is associated with high complication rates. ECMO induces systemic inflammation and endothelial hyperpermeability, thereby causing tissue edema, microcirculatory perfusion disturbances, and organ failure. This study investigated whether the inhibition of vascular endothelial protein tyrosine phosphatase (VE-PTP), a regulator of endothelial permeability, reduces extracorporeal circulation (ECC)-induced microvascular dysfunction. Rats were subjected to ECC after treatment with Razuprotafib (n = 11) or a placebo (n = 11), or they underwent a sham procedure (n = 8). Razuprotafib had no effect on the ECC-induced impairment of capillary perfusion, as assessed with intravital microscopy, nor did it influence the increased wet-to-dry weight ratio in kidneys, a marker of edema associated with ECC. Interestingly, Razuprotafib suppressed the ECC-induced increase in TNFα, whereas angiopoietin-2 even further increased, following the discontinuation of ECC. Circulating interleukin-6, ICAM-1, angiopoietin-1, and soluble Tie2 and tissue VE-PTP, Tie1, and Tie2 mRNA expression were not affected by Razuprotafib. Furthermore, Razuprotafib improved the PaO2/FiO2 ratio and reduced histopathological pulmonary interstitial inflammation following ECC compared to the placebo. To conclude, treatment with Razuprotafib did not improve ECC-induced microcirculatory perfusion disturbances nor renal edema. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Acute Lung Injury)
►▼ Show Figures

Figure 1

31 pages, 5222 KiB  
Article
Chitosan Nanoparticle-Encapsulated Cordyceps militaris Grown on Germinated Rhynchosia nulubilis Reduces Type II Alveolar Epithelial Cell Apoptosis in PM2.5-Induced Lung Injury
by Hyo-Min Kim, Jong-Heon Kim, Byung-Jin Park and Hye-Jin Park
Int. J. Mol. Sci. 2025, 26(3), 1105; https://doi.org/10.3390/ijms26031105 - 27 Jan 2025
Viewed by 1049
Abstract
Chitosan nanoparticles (CNPs) were synthesized in this study to enhance the limited bioactivity and stability of Cordyceps militaris grown on germinated Rhynchosia nulubilis (GRC) and effectively deliver it to target tissues. Under optimized conditions, stable encapsulation of GRC was achieved by setting the [...] Read more.
Chitosan nanoparticles (CNPs) were synthesized in this study to enhance the limited bioactivity and stability of Cordyceps militaris grown on germinated Rhynchosia nulubilis (GRC) and effectively deliver it to target tissues. Under optimized conditions, stable encapsulation of GRC was achieved by setting the chitosan (CHI)-to-tripolyphosphate (TPP) ratio to 4:1 and adjusting the pH of TPP to 2, resulting in a zeta potential of +22.77 mV, which indicated excellent stability. As the concentration of GRC increased, the encapsulation efficiency decreased, whereas the loading efficiency increased. Fourier-transform infrared (FT-IR) spectroscopy revealed shifts in the amide I and II bands of CHI from 1659 and 1578 to 1639 cm⁻1, indicating hydrogen bonding and successful encapsulation of GRC encapsulated with CNPs (GCN). X-ray diffraction (XRD) examination revealed the transition of the nanoparticles from a crystalline to an amorphous state, further confirming successful encapsulation. In vivo experiments demonstrated that GCN treatment significantly reduced lung injury scores in fine particulate matter (PM2.5)-exposed mice (p < 0.05) and alleviated lung epithelial barrier damage by restoring the decreased expression of occludin protein (p < 0.05). In addition, GCN decreased the PM2.5-induced upregulation of MMP-9 and COL1A1 mRNA expression levels, preventing extracellular matrix (ECM) degradation and collagen accumulation (p < 0.05). GCN exhibited antioxidant effects by reducing the mRNA expression of nitric oxide synthase (iNOS) and enhancing both the protein and mRNA expression of superoxide dismutase (SOD-1) caused by PM2.5, thereby alleviating oxidative stress (p < 0.05). In A549 cells, GCN significantly reduced PM2.5-induced reactive oxygen species (ROS) production compared with GRC (p < 0.05), with enhanced intracellular uptake confirmed using fluorescence microscopy (p < 0.05). In conclusion, GCN effectively alleviated PM2.5-induced lung damage by attenuating oxidative stress, suppressing apoptosis, and preserving the lung epithelial barrier integrity. These results emphasize its potential as a therapeutic candidate for preventing and treating the lung diseases associated with PM2.5 exposure. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Acute Lung Injury)
►▼ Show Figures

Figure 1

10 pages, 2779 KiB  
Article
Surfactant Phospholipid Kinetics in Ventilated Children after Therapeutic Surfactant Supplementation
by Victoria M. Goss, Ahilanandan Dushianthan, Jenni McCorkell, Katy Morton, Kevin C. W. Goss, Michael J. Marsh, John V. Pappachan and Anthony D. Postle
Int. J. Mol. Sci. 2024, 25(19), 10480; https://doi.org/10.3390/ijms251910480 - 29 Sep 2024
Viewed by 953
Abstract
Acute lung Injury leads to alterations in surfactant lipid composition and metabolism. Although several mechanisms contribute to dysregulated surfactant metabolism, studies investigating in vivo surfactant metabolism are limited. The aim of this study is to characterise surfactant phospholipid composition and flux utilising a [...] Read more.
Acute lung Injury leads to alterations in surfactant lipid composition and metabolism. Although several mechanisms contribute to dysregulated surfactant metabolism, studies investigating in vivo surfactant metabolism are limited. The aim of this study is to characterise surfactant phospholipid composition and flux utilising a stable isotope labelling technique in mechanically ventilated paediatric patients. Paediatric patients (<16 years of age) received 3.6 mg/kg intravenous methyl-D9-choline chloride followed by the endotracheal instillation of 100 mg/kg of exogenous surfactant after 24 h. Bronchioalveolar fluid samples were taken at baseline and 12, 24, 36, 48, 72 and 96 h after methyl-D9-choline infusion. Nine participants (median age of 48 days) were recruited. The primary phosphatidylcholine (PC) composition consisted of PC16:0/16:0 or DPPC (32.0 ± 4.5%). Surfactant supplementation resulted in a 30% increase in DPPC. Methyl-D9 PC enrichment was detected after 12 h and differed significantly between patients, suggesting variability in surfactant synthesis/secretion by the CDP-choline pathway. Peak enrichment was achieved (0.94 ± 0.15% of total PC) at 24 h after methyl-D9-choline infusion. There was a trend towards reduced enrichment with the duration of mechanical ventilation prior to study recruitment; however, this was not statistically significant (p = 0.19). In this study, we demonstrated the fractional molecular composition and turnover of surfactant phospholipids, which was highly variable between patients. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Acute Lung Injury)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop