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Biomedicines
Special Issues
Advanced Research in Lung Injury and Lung Fibrosis
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Advanced Research in Lung Injury and Lung Fibrosis

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 3820

Special Issue Editors

Dr. Chao He

E-Mail Website
Guest Editor
Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, AL, USA
Interests: pulmonary fibrosis; macrophages; metabolism; early phase drug discovery
Dr. Huachun Cui

E-Mail Website
Guest Editor
Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, AL, USA
Interests: inflammation; non-coding RNAs; cellular metabolism in lung injury and fibrosis
Dr. Pulin Che

E-Mail Website
Guest Editor
Department of Anesthesiology and Perioperative Medicin, Division of Molecular and Translational Biomedicine, University of Alabama at Birmingham, Birmingham, AL, USA
Interests: lung fibrosis; tissue injury and remodeling

Special Issue Information

Dear Colleagues,

The persistent activation of immune cells such as neutrophils and macrophages is the hallmark of acute and chronic lung injury, leading to alveolar epithelial cell death and the impairment of gas exchange. However, immune cells also secrete growth factors critical for epithelial cell and fibroblast proliferation as well as differentiation to facilitate the repair. Dysregulated lung repair can lead to pulmonary fibrosis, a devastating disease currently without effective treatment. The most common one, idiopathic pulmonary fibrosis (IPF), has a medium survival time of 3–5 years. Thus, understanding the dynamic crosstalk between these cells could help to identify new therapeutic targets for both lung injury and pulmonary fibrosis. We invite you to submit original research articles or relevant topic reviews on lung injury and fibrosis, focusing on intercellular crosstalk and metabolism.

Dr. Chao He
Dr. Huachun Cui
Dr. Pulin Che
Guest Editors

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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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 injury
  • pulmonary fibrosis
  • lung macrophages
  • lung fibroblasts
  • alveolar epithelial cells
  • non-coding RNAs
  • metabolism
  • oxidative stress

Published Papers (2 papers)

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Research

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20 pages, 5753 KiB  
Article
Hesperidin Attenuates Hypothyroidism-Induced Lung Damage in Adult Albino Rats by Modulating Oxidative Stress, Nuclear Factor Kappa-B Pathway, Proliferating Cell Nuclear Antigen and Inflammatory Cytokines
by Walaa Hegazy, Hader I. Sakr, Manal Abdul Hamid, Mohamed A. Abdelaziz, Marwa Salah, Eman S. Abdel Rehiem and Adel Abdel Moneim
Biomedicines 2023, 11(6), 1570; https://doi.org/10.3390/biomedicines11061570 - 29 May 2023
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Abstract
The occurrence of worsening pulmonary function has been connected to hypothyroidism (HPO). Hesperidin (HES) was suggested to have antioxidant, anti-proliferative, and anti-inflammatory potential. Our study’s objective was to determine whether HES could reduce carbimazole (CBZ)-induced lung injury more effectively than Eltroxin (ELT) in [...] Read more.
The occurrence of worsening pulmonary function has been connected to hypothyroidism (HPO). Hesperidin (HES) was suggested to have antioxidant, anti-proliferative, and anti-inflammatory potential. Our study’s objective was to determine whether HES could reduce carbimazole (CBZ)-induced lung injury more effectively than Eltroxin (ELT) in adult male albino rats or not. At random, 32 rats were distributed into four groups: Group I: normal control, to induce HPO, the remaining three groups were given CBZ (20 mg/kg/day) dissolved in distilled water for 1 week. They were then split up into three groups. Group II: orally administered CBZ (20 mg/kg b.w in water/day), Group III: HES (200 mg/kg/day) dissolved in 1% carboxymethyl-cellulose + CBZ treated, and Group IV: ELT (0.045 mg/kg/day) dissolved in distilled water + CBZ treated. All treatments were delivered for 12 weeks. Blood was collected to assess thyroid-stimulating hormone (TSH) and thyroid hormones (THs). Lung injury was evaluated based on the pulmonary content of interleukin (IL)-35, IL-6, and tumor necrosis factor-alpha (TNF-α), along with the estimation of lipid peroxidation, catalase, glutathione levels, superoxide dismutase, heme oxygenase-1 (HO-1), and nuclear factor erythroid 2-related factor 2 (Nrf2). The histological, ultrastructural, and immunohistochemical study of nuclear factor Kappa-B (NF-κB) and inducible nitric oxide synthase (iNOS), together with estimating the proliferation of cells using Antigen Ki-67 in lung tissue were performed. HES and ELT primarily suppressed variable lung damage mechanisms by suppressing TSH, the NF-κB/TNF-α pathway, iNOS, lipid peroxidation, Ki-67, and inflammatory mediators. On the other hand, they improved THs, antioxidant parameters, and the Nrf2/HO-1 pathway. HES and ELT exhibited an ameliorative effect that was reflected in the histopathological, immunohistochemical, and ultrastructural results. These results indicate that HES is a pneumoprotective agent that could be a promising treatment for oxidative stress, inflammation, and proliferation. Full article
(This article belongs to the Special Issue Advanced Research in Lung Injury and Lung Fibrosis)
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Review

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12 pages, 928 KiB  
Review
Cell Adhesion Molecules in Fibrotic Diseases
by Qianjiang Hu, Komal Saleem, Jyotsana Pandey, Arzoo N. Charania, Yong Zhou and Chao He
Biomedicines 2023, 11(7), 1995; https://doi.org/10.3390/biomedicines11071995 - 14 Jul 2023
Cited by 3 | Viewed by 1916
Abstract
Mechanisms underlying the pathogenesis of tissue fibrosis remain incompletely understood. Emerging evidence suggests that cell adhesion molecules (CAMs) are critical in fibrotic progression in many organs, including lung, kidney, skin, and liver. CAMs promote cell–cell and cell–extracellular matrix (ECM) interactions to maintain tissue [...] Read more.
Mechanisms underlying the pathogenesis of tissue fibrosis remain incompletely understood. Emerging evidence suggests that cell adhesion molecules (CAMs) are critical in fibrotic progression in many organs, including lung, kidney, skin, and liver. CAMs promote cell–cell and cell–extracellular matrix (ECM) interactions to maintain tissue architecture and normal function in homeostasis. However, dysregulated expression and function of CAMs can lead to chronic inflammation and tissue fibrosis. The major families of CAMs include integrins, cadherins, selectins, and immunoglobulins. Here, we review the role of the CAMs in fibrosis development across various organs with a focus on integrins and cadherins, and discuss their respective roles in the development of pulmonary fibrosis. Full article
(This article belongs to the Special Issue Advanced Research in Lung Injury and Lung Fibrosis)
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