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Life
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Deciphering Antioxidant Defence Mechanisms in Neuronal and Non-neuronal Cells
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Deciphering Antioxidant Defence Mechanisms in Neuronal and Non-neuronal Cells

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (16 February 2024) | Viewed by 3030

Special Issue Editors

Dr. Paolo Rosa

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Guest Editor
Department of Medical-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome, Italy
Interests: brain aging; neurodegenerative diseases; glioblastoma; hypoxia
Special Issues, Collections and Topics in MDPI journals
Dr. Alessio Crestini

E-Mail Website
Guest Editor
Department of Neuroscience, Istituto Superiore di Sanità (ISS), Rome, Italy
Interests: neurodegeneration; Alzheimer’s disease; genetics of dementia; oxidative stress; microRNAs
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Throughout life, the brain is constantly exposed to injuries that can exacerbate degenerative processes and accelerate aging. Oxidative stress is a deleterious condition defined as the imbalance between oxidant and antioxidant defences leading to reactive oxygen species (ROS) generation, which  oxidizes macromolecules such as lipids, proteins and nucleic acids causing cell death and leading to neurodegeneration. Therefore, cells have evolved defence mechanisms to limit oxidative stress damage and maintain redox homeostasis. Understanding the physiological function of brain cells in response to oxidative injuries, as well as how the crosstalk between neuronal and glial cells is influenced by this condition will be of fundamental importance for the development of new therapeutic interventions focused on limiting oxidative brain injury.

Therefore, in this Special Issue, we invite investigators to contribute with original research articles, as well as review articles focusing on the role of oxidative stress in the pathophysiology of brain aging and neurodegenerative disorders, highlighting the molecular mechanisms of antioxidant defence in neuronal and non-neuronal cells. Understanding the control of redox homeostasis in normal and pathological conditions will be of fundamental importance in tackling brain diseases.

Potential topics include, but are not limited to, the following:

  • Molecular basis of oxidative stress on glial cells in the aging brain;
  • Neurodegenerative diseases and oxidative stress: the role of glial cells;
  • Effects of oxidative stress on lipid metabolism in neurodegenerative diseases;
  • Mechanisms of hypoxia-induced oxidative stress in neuronal and non-neuronal cells in neurodegenerative diseases;
  • Role of oxidative stress-induced autophagy in neuroprotection;
  • Oxidative stress-induced microglial activation in brain aging and neurodegeneration;
  • Discovery of novel synthetic antioxidants to limit oxidative stress in the brain;
  • Molecular mechanisms of antioxidants in brain aging and neurodegeneration;
  • Mechanisms of astrocyte reactivity to oxidative stress in the brain;
  • Microglial activation and neurodegenerative diseases: understanding the molecular basis of oxidative stress;
  • The role of astrocyte response to oxidative stress in BBB permeability.

You may choose our Joint Special Issue in Brain Sciences.

Dr. Paolo Rosa
Dr. Alessio Crestini
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. Life 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

  • oxidative stress
  • reactive oxygen species
  • ROS
  • brain aging
  • neurodegeneration
  • neuronal loss
  • hypoxia
  • glial cells
  • microglia
  • antioxidants

Published Papers (2 papers)

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Research

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21 pages, 3654 KiB  
Article
In Vitro Evaluation of the Antioxidant Capacity of 3,3-Disubstituted-3H-benzofuran-2-one Derivatives in a Cellular Model of Neurodegeneration
by Sofia Scibetta, Martina Miceli, Marco Iuliano, Luca Stefanuto, Elena Carbone, Paola Piscopo, Vincenzo Petrozza, Giovanna Romeo, Giorgio Mangino, Antonella Calogero, Tecla Gasperi and Paolo Rosa
Life 2024, 14(4), 422; https://doi.org/10.3390/life14040422 - 22 Mar 2024
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Abstract
Oxidative stress represents a hallmark for many degenerative pathologies of the Central Nervous System. Throughout life, the constant pressure of noxious stimuli and/or episodes of traumatic events may expose the brain to a microenvironment where the non-balanced reactive oxygen species inevitably lead to [...] Read more.
Oxidative stress represents a hallmark for many degenerative pathologies of the Central Nervous System. Throughout life, the constant pressure of noxious stimuli and/or episodes of traumatic events may expose the brain to a microenvironment where the non-balanced reactive oxygen species inevitably lead to neuronal loss and cognitive decline. HO-1, a 32 kDa heat-shock protein catalyzing the degradation of heme into carbon monoxide (CO), iron and biliverdin/bilirubin is considered one of the main antioxidant defense mechanisms playing pivotal roles in neuroprotection. Restoring the redox homeostasis is the goal of many natural or synthetic antioxidant molecules pursuing beneficial effects on brain functions. Here, we investigated the antioxidant capacity of four selected benzofuran-2-one derivatives in a cellular model of neurodegeneration represented by differentiated SH-SY5Y cells exposed to catechol-induced oxidative stress. Our main results highlight how all the molecules have antioxidant properties, especially compound 9, showing great abilities in reducing intracellular ROS levels and protecting differentiated SH-SY5Y cells from catechol-induced death. This compound above all seems to boost HO-1 mRNA and perinuclear HO-1 protein isoform expression when cells are exposed to the oxidative insult. Our findings open the way to consider benzofuran-2-ones as a novel and promising adjuvant antioxidant strategy for many neurodegenerative disorders. Full article
(This article belongs to the Special Issue Deciphering Antioxidant Defence Mechanisms in Neuronal and Non-neuronal Cells)
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Review

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19 pages, 2219 KiB  
Review
Influence of Alcohol on Intracerebral Hemorrhage: From Oxidative Stress to Glial Cell Activation
by Shaik Ismail Mohammed Thangameeran, Po-Kai Wang, Hock-Kean Liew and Cheng-Yoong Pang
Life 2024, 14(3), 311; https://doi.org/10.3390/life14030311 - 27 Feb 2024
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Abstract
The intricate relationship between alcohol consumption and intracerebral hemorrhage (ICH) presents a nuanced field of study, especially concerning the dose-dependent impact on secondary brain injury (SBI). Recognizing the established risks associated with heavy drinking, this review delves deeper into the less understood territories [...] Read more.
The intricate relationship between alcohol consumption and intracerebral hemorrhage (ICH) presents a nuanced field of study, especially concerning the dose-dependent impact on secondary brain injury (SBI). Recognizing the established risks associated with heavy drinking, this review delves deeper into the less understood territories of low to moderate alcohol consumption. By systematically analyzing recent studies, we uncover critical insights into how varying alcohol intake levels modulate ICH risk through mechanisms such as microglial activation, oxidative stress, and the protective potential of polyphenols. This analysis extends beyond the hypertensive effects of heavy alcohol use to explore the complex molecular pathophysiology involved in alcohol-related ICH. Our findings indicate that while heavy alcohol use unequivocally exacerbates ICH risk, moderate consumption and its associated polyphenols may offer neuroprotective effects against SBI, albeit within a finely balanced threshold. This review highlights the significant gaps in current understanding and underscores the urgent need for targeted research to elucidate these complex interactions. Through this comprehensive examination, we aim to inform more nuanced public health policies and intervention strategies, taking into account the diverse effects of alcohol consumption on ICH risk. Full article
(This article belongs to the Special Issue Deciphering Antioxidant Defence Mechanisms in Neuronal and Non-neuronal Cells)
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