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Molecular Mechanisms of Acute Lung Injury
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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 Biology".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 2613

Special Issue Editor

Dr. Tamás Jilling

E-Mail Website
Guest Editor
Department of Pediatrics, University of Alabama at Birmingham School of Medicine, 1700 6th Avenue South, Birmingham, AL 35233, USA
Interests: lung injury; pregnancy; preeclampsia; bronchopulmonary displasia

Special Issue Information

Dear Colleagues,

This Special Issue is dedicated to articles related to the mechanisms and treatment of acute lung injury. Acute lung injury can be caused by direct injury to the lung via the inhalation of toxic gases or smoke, bacterial or viral infection, aspiration of gastric content, pulmonary contusion, alveolar hemorrhage, among other causes. Acute lung injury may also occur via indirect injury to the lung in the case of sepsis, pancreatitis, blood transfusion, hemolysis by multiple causes, and other forms of systemic injury/inflammatory processes. With the exception of a few specialized conditions wherein the underlying condition that causes the lung injury can be treated, there is currently no specific treatment for acute lung injury, and generalized supportive care is employed until the lung injury is resolved. Therefore, further exploration of the mechanisms involved in acute lung injury and therapeutic targeting of newly discovered mechanisms is warranted. For this Special Issue, we invite both original research articles as well as comprehensive reviews addressing mechanisms of acute lung injury and novel therapeutic strategies. Examples of potential topics include:

  • Novel models of acute lung injury;
  • Mechanisms and treatment of SARS-Cov-2-induced acute lung injury;
  • Mechanisms and treatment of influenza-virus-induced acute lung injury;
  • Acute lung injury in vulnerable populations: pediatric, geriatric, pregnant, underlying conditions;
  • Mechanisms and treatment of acute lung injury caused by toxic gases;
  • Acute lung injury following cutaneous burn: thermal, chemical, electrical;
  • The role of non-encapsulated heme in acute lung injury: hemorrhage, hemolysis, sickle cell disease, other hemoglobinopathies;
  • Heme elimination strategies for the treatment of acute lung injury;
  • Sepsis-associated acute lung injury;
  • Acute lung injury following aspiration.

Dr. Tamás Jilling
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
  • mechanism
  • toxic gas
  • burn
  • sepsis
  • aspiration
  • free heme

Published Papers (2 papers)

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Research

15 pages, 9197 KiB  
Article
TRPC6 Deletion Enhances eNOS Expression and Reduces LPS—Induced Acute Lung Injury
by Mengyuan Wang, Xingfang Zhang, Juan Guo, Shangze Yang, Fang Yang and Xingjuan Chen
Int. J. Mol. Sci. 2023, 24(23), 16756; https://doi.org/10.3390/ijms242316756 - 25 Nov 2023
Cited by 1 | Viewed by 1037
Abstract
Acute lung injury (ALI) is characterized by endothelial barrier disruption and associated inflammatory responses, and transient receptor potential cation channel 6 (TRPC6)—mediated Ca2+ influx is critical for endothelial hyperpermeability. In this study, we investigated the role of TRPC6 in LPS—induced ALI, analyzed [...] Read more.
Acute lung injury (ALI) is characterized by endothelial barrier disruption and associated inflammatory responses, and transient receptor potential cation channel 6 (TRPC6)—mediated Ca2+ influx is critical for endothelial hyperpermeability. In this study, we investigated the role of TRPC6 in LPS—induced ALI, analyzed gene expression in WT and TRPC6-/- lungs using RNA sequencing, and explored the effects of TRPC6 in the LPS—induced hyperpermeability in human umbilical vein endothelial cells (HUVECs) to elucidate the underlying mechanisms. Intratracheal instillation of LPS caused edema in the mouse lungs. Deletion of TRPC6 reduced LPS—induced lung edema and decreased cell infiltration. RNA sequencing analysis suggested that downregulated cell adhesion molecules in TRPC6-/- lungs may be responsible for their resistance to LPS—induced injury. In addition, downregulation of TRPC6 significantly alleviated the LPS—induced decrease in eNOS expression in lung tissue as well as in HUVECs. Moreover, inhibition of TRPC6 with the channel antagonist larixyl led to a decrease in LPS—induced hyperpermeability and ROS production in HUVECs, which could be reversed by blocking eNOS. Our findings suggest that inhibition of TRPC6 ameliorates LPS—induced ALI, which may be achieved by acting on the cell adhesion molecule signaling pathway and participating in the regulation of eNOS levels in endothelial cells. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Acute Lung Injury)
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11 pages, 477 KiB  
Article
The Presence of T Allele (rs35705950) of the MUC5B Gene Predicts Lower Baseline Forced Vital Capacity and Its Subsequent Decline in Patients with Hypersensitivity Pneumonitis
by Katarzyna B. Lewandowska, Monika Szturmowicz, Urszula Lechowicz, Monika Franczuk, Katarzyna Błasińska, Maria Falis, Kamila Błaszczyk, Małgorzata Sobiecka, Dorota Wyrostkiewicz, Izabela Siemion-Szcześniak, Małgorzata Bartosiewicz, Piotr Radwan-Röhrenschef, Adriana Roży, Joanna Chorostowska-Wynimko and Witold Z. Tomkowski
Int. J. Mol. Sci. 2023, 24(13), 10748; https://doi.org/10.3390/ijms241310748 - 28 Jun 2023
Cited by 2 | Viewed by 1136
Abstract
Hypersensitivity pneumonitis (HP) is an exposure-related interstitial lung disease with two phenotypes—fibrotic and non-fibrotic. Genetic predisposition is an important factor in the disease pathogenesis and fibrosis development. Several genes are supposed to be associated with the fibrosing cascade in the lungs. One of [...] Read more.
Hypersensitivity pneumonitis (HP) is an exposure-related interstitial lung disease with two phenotypes—fibrotic and non-fibrotic. Genetic predisposition is an important factor in the disease pathogenesis and fibrosis development. Several genes are supposed to be associated with the fibrosing cascade in the lungs. One of the best-recognized and most prevalent is the common MUC5B gene promoter region polymorphism variant rs35705950. The aim of our study was to establish the frequency of the minor allele of the MUC5B gene in the population of patients with HP and to find the relationship between the MUC5B promoter region polymorphism and the development of lung fibrosis, the severity of the disease course, and the response to the treatment in patients with HP. Eighty-six consecutive patients with HP were tested for the genetic variant rs35705950 of the MUC-5B gene. Demographic, radiological, and functional parameters were collected. The relationship between the presence of the T allele and lung fibrosis, pulmonary function test parameters, and the treatment response were analyzed. The minor allele frequency in the study group was 17%, with the distribution of the genotypes GG in 69.8% of subjects and GT/TT in 30.2%. Patients with the GT/TT phenotype had significantly lower baseline forced vital capacity (FVC) and significantly more frequently had a decline in FVC with time. The prevalence of lung fibrosis in high-resolution computed tomography (HRCT) was not significantly increased in GT/TT variant carriers compared to GG ones. The patients with the T allele tended to respond worse to immunomodulatory treatment and more frequently received antifibrotic drugs. In conclusions: The frequency of MUC5B polymorphism in HP patients is high. The T allele may indicate a worse disease course, worse immunomodulatory treatment response, and earlier need for antifibrotic treatment. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Acute Lung Injury)
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