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Signalling Pathway and Regulation of Oxidative Stress in Lung Diseases

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: 31 May 2024 | Viewed by 1431

Special Issue Editors


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Guest Editor
Institute of Translational Pharmacology (IFT)-CNR, 90153 Rome, Italy
Interests: lung disease; oxidative stress; innate immunity; drug delivery; experimental pharmacology; oxidative stress sensors

E-Mail Website
Guest Editor
Institute of Translational Pharmacology (IFT) - National Research Council of Italy (CNR), 90153 Palermo, Italy
Interests: translational pulmonology; immunopathology of lung disease; experimental pharmacology; innate immunity; oxidative stress sensors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In the lungs, airway epithelium is the first line of defense against inhaled particles (or inhalants). Exposure to cigarette smoke, allergens, viruses and other environmental contaminants increases airway oxidative stress. Airway epithelium has a central role in the physiopathology of chronic airway diseases, notably asthma and COPD. Increased oxidative stress is associated with the amplification of inflammatory process, tissue damage and alteration of innate and adaptive immunity, thus compromising airway homeostasis. Airway epithelium is a primary target of the anti-inflammatory actions of glucocorticoids. Cigarette smoke and oxidative stress negatively affect pathways associated with steroid response, whereas antioxidants and drugs effective in reducing oxidative stress enhance the response of steroids. This Special Issue will explore the pathways activated by oxidative stress, with particular focus on the mechanisms associated with corticoresistance, with the aim of identifying new pharmacological strategies capable of restoring the oxidant/antioxidant balance.

Dr. Maria Ferraro
Dr. Elisabetta Pace
Guest Editors

Manuscript Submission Information

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Keywords

  • oxidative stress
  • lung disease
  • airway epithelium
  • steroid resistance
  • antioxidant treatment

Published Papers (1 paper)

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Research

14 pages, 2308 KiB  
Article
Formoterol Exerts Anti-Cancer Effects Modulating Oxidative Stress and Epithelial-Mesenchymal Transition Processes in Cigarette Smoke Extract Exposed Lung Adenocarcinoma Cells
by Maria Ferraro, Serena Di Vincenzo, Valentina Lazzara, Paola Pinto, Bernardo Patella, Rosalinda Inguanta, Andreina Bruno and Elisabetta Pace
Int. J. Mol. Sci. 2023, 24(22), 16088; https://doi.org/10.3390/ijms242216088 - 08 Nov 2023
Cited by 1 | Viewed by 995
Abstract
Lung cancer frequently affects patients with Chronic Obstructive Pulmonary Disease (COPD). Cigarette smoke (CS) fosters cancer progression by increasing oxidative stress and by modulating epithelial-mesenchymal transition (EMT) processes in cancer cells. Formoterol (FO), a long-acting β2-agonist widely used for the treatment of COPD, [...] Read more.
Lung cancer frequently affects patients with Chronic Obstructive Pulmonary Disease (COPD). Cigarette smoke (CS) fosters cancer progression by increasing oxidative stress and by modulating epithelial-mesenchymal transition (EMT) processes in cancer cells. Formoterol (FO), a long-acting β2-agonist widely used for the treatment of COPD, exerts antioxidant activities. This study explored in a lung adenocarcinoma cell line (A549) whether FO counteracted the effects of cigarette smoke extract (CSE) relative to oxidative stress, inflammation, EMT processes, and cell migration and proliferation. A549 was stimulated with CSE and FO, ROS were evaluated by flow-cytometry and by nanostructured electrochemical sensor, EMT markers were evaluated by flow-cytometry and Real-Time PCR, IL-8 was evaluated by ELISA, cell migration was assessed by scratch and phalloidin test, and cell proliferation was assessed by clonogenic assay. CSE significantly increased the production of ROS, IL-8 release, cell migration and proliferation, and SNAIL1 expression but significantly decreased E-cadherin expression. FO reverted all these phenomena in CSE-stimulated A549 cells. The present study provides intriguing evidence that FO may exert anti-cancer effects by reverting oxidative stress, inflammation, and EMT markers induced by CS. These findings must be validated in future clinical studies to support FO as a valuable add-on treatment for lung cancer management. Full article
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