Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.8
5.6
Journals
IJMS
Special Issues
Oxidative Stress and Brain Injury 3.0
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Oxidative Stress and Brain Injury 3.0

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: closed (30 June 2023) | Viewed by 10686

Special Issue Editor

Prof. Dr. Vittorio Fineschi

E-Mail Website
Guest Editor
Department of Anatomical, Histological, Forensic and Orthopaedic Sciences, Sapienza University of Rome, Viale Regina Elena 336, 00161 Rome, RM, Italy
Interests: forensic pathology; sudden cardiac death; molecular mechanisms; traumatic brain injury & oxidative stress; immunohistochemistry; drugs of abuse; oxidative stress; maternal mortality; miRNA; forensic pathologies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our previous Special Issue “Oxidative Stress and Brain Injury” and "Oxidative Stress and Brain Injury 2.0"

The scientific literature has given extensive prominence to the effects of reactive oxygen species (ROS) and their induction of oxidative stress and fatal effects on the brain following injury by endogenous factors, traumatic brain injury, and degenerative neural injury due to ROS. Oxidative stress is an event caused by an imbalance between biochemical processes, leading to the production of ROS and those elements responsible for the removal of ROS, known as the enzymatic and non-enzymatic antioxidant cellular defense systems. The excessive production of ROS due to excitotoxicity and depletion of the endogenous antioxidant system induces peroxidation of cellular and vascular structures, protein oxidation, and inhibition of the mitochondrial electron transport chain, causing oxidative cellular damage. Oxidative stress induces cell membrane lipoperoxidation and calcium release, which activates calpain. ROS and RNS induce oxidative damage in neuronal mitochondria and compromise Ca2+ homeostasis. Increase in the defense mechanisms using exogenous antioxidants may be neuroprotective, particularly if they are given within the neuroprotective time window. As an example, a promising potential therapeutic target in DAI is to directly address mitochondria-related injury or to modulate energetic axonal energy failure. However, dietary supplementation with antioxidants and the use of pharmacological agents targeting oxidative stress seem logical, but the benefits of proven antioxidant strategies have not been clearly demonstrated to date.

In this Special Issue on “Oxidative Stress and Brain Injury”, we invite front-line researchers and investigators to submit original research and review articles regarding topics including but not limited to:

  • Measurement of ROS;
  • Pathology of brain injuries;
  • Traumatic brain injuries;
  • Hypoxic–ischemic brain damage;
  • Experimental models of brain injury;
  • Targeted therapy of brain injuries;
  • Drug abuse and ROS;
  • Histological diagnosis of brain injuries;
  • Epigenetics of brain injuries;
  • miRNA and prognosis of neural damage;
  • Novel approaches and proofs of principle in therapy;
  • Quality of life after brain injury.

Prof. Dr. Vittorio Fineschi
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.

Published Papers (5 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

Jump to: Review

23 pages, 5932 KiB  
Article
Antidiabetic Drugs Can Reduce the Harmful Impact of Chronic Smoking on Post-Traumatic Brain Injuries
by Farzane Sivandzade, Faleh Alqahtani, Hemangini Dhaibar, Diana Cruz-Topete and Luca Cucullo
Int. J. Mol. Sci. 2023, 24(7), 6219; https://doi.org/10.3390/ijms24076219 - 25 Mar 2023
Viewed by 1691
Abstract
Traumatic Brain Injury (TBI) is a primary cause of cerebrovascular and neurological disorders worldwide. The current scientific researchers believe that premorbid conditions such as tobacco smoking (TS) can exacerbate post-TBI brain injury and negatively affect recovery. This is related to vascular endothelial dysfunction [...] Read more.
Traumatic Brain Injury (TBI) is a primary cause of cerebrovascular and neurological disorders worldwide. The current scientific researchers believe that premorbid conditions such as tobacco smoking (TS) can exacerbate post-TBI brain injury and negatively affect recovery. This is related to vascular endothelial dysfunction resulting from the exposure to TS-released reactive oxygen species (ROS), nicotine, and oxidative stress (OS) stimuli impacting the blood–brain barrier (BBB) endothelium. Interestingly, these pathogenic modulators of BBB impairment are similar to those associated with hyperglycemia. Antidiabetic drugs such as metformin (MF) and rosiglitazone (RSG) were shown to prevent/reduce BBB damage promoted by chronic TS exposure. Thus, using in vivo approaches, we evaluated the effectiveness of post-TBI treatment with MF or RSG to reduce the TS-enhancement of BBB damage and brain injury after TBI. For this purpose, we employed an in vivo weight-drop TBI model using male C57BL/6J mice chronically exposed to TS with and without post-traumatic treatment with MF or RSG. Our results revealed that these antidiabetic drugs counteracted TS-promoted downregulation of nuclear factor erythroid 2-related factor 2 (NRF2) expression and concomitantly dampened TS-enhanced OS, inflammation, and loss of BBB integrity following TBI. In conclusion, our findings suggest that MF and RSG could reduce the harmful impact of chronic smoking on post-traumatic brain injuries. Full article
(This article belongs to the Special Issue Oxidative Stress and Brain Injury 3.0)
►▼ Show Figures

Figure 1

11 pages, 2647 KiB  
Communication
The Expression of FOXO3a as a Forensic Diagnostic Tool in Cases of Traumatic Brain Injury: An Immunohistochemical Study
by Aniello Maiese, Federica Spina, Giacomo Visi, Fabio Del Duca, Alessandra De Matteis, Raffaele La Russa, Marco Di Paolo, Paola Frati and Vittorio Fineschi
Int. J. Mol. Sci. 2023, 24(3), 2584; https://doi.org/10.3390/ijms24032584 - 30 Jan 2023
Cited by 6 | Viewed by 1464
Abstract
Traumatic brain injury (TBI) is one of the most well-known causes of neurological impairment and disability in the world. The Forkhead Box class O (FOXO) 3a is a transcription factor that is involved in different molecular processes, such as cell apoptosis regulation, neuroinflammation [...] Read more.
Traumatic brain injury (TBI) is one of the most well-known causes of neurological impairment and disability in the world. The Forkhead Box class O (FOXO) 3a is a transcription factor that is involved in different molecular processes, such as cell apoptosis regulation, neuroinflammation and the response to oxidative stress. This study is the first to evaluate the post-mortem immunohistochemical (IHC) positivity of FOXO3a expression in human cases of TBI deaths. The autopsy databases of the Legal Medicine and Forensic Institutes of the “Sapienza” University of Roma and the University of Pisa were retrospectively reviewed. After analyzing autopsy reports, 15 cases of TBI deaths were selected as the study group, while the other 15 cases were chosen among non-traumatic brain deaths as the control group. Decomposed bodies and those with initial signs of putrefaction were excluded. Routine histopathological studies were performed using hematoxylin–eosin (H&E) staining. Furthermore, an IHC investigation on cerebral samples was performed. To evaluate FOXO3a expression, anti-FOXO3a antibodies (GTX100277) were utilized. Concerning the IHC analysis, all 15 samples of TBI cases showed positivity for FOXO3a in the cerebral parenchyma. All control cerebral specimens showed FOXO3a negativity. In addition, the longer the survival time, the greater the positivity to the reaction with FOXO3a was. This study shows the important role of FOXO3a in neuronal autophagy and apoptosis regulation and suggests FOXO3a as a possible potential pharmacological target. Full article
(This article belongs to the Special Issue Oxidative Stress and Brain Injury 3.0)
►▼ Show Figures

Figure 1

Review

Jump to: Research

14 pages, 997 KiB  
Review
Old and Promising Markers Related to Autophagy in Traumatic Brain Injury
by Tommaso Livieri, Calogero Cuttaia, Raffaella Vetrini, Monica Concato, Michela Peruch, Margherita Neri, Davide Radaelli and Stefano D’Errico
Int. J. Mol. Sci. 2023, 24(1), 72; https://doi.org/10.3390/ijms24010072 - 21 Dec 2022
Cited by 5 | Viewed by 1471
Abstract
Traumatic brain injury (TBI) is one of the first causes of death and disability in the world. Because of the lack of macroscopical or histologic evidence of the damage, the forensic diagnosis of TBI could be particularly difficult. Considering that the activation of [...] Read more.
Traumatic brain injury (TBI) is one of the first causes of death and disability in the world. Because of the lack of macroscopical or histologic evidence of the damage, the forensic diagnosis of TBI could be particularly difficult. Considering that the activation of autophagy in the brain after a TBI is well documented in literature, the aim of this review is to find all autophagy immunohistological protein markers that are modified after TBI to propose a method to diagnose this eventuality in the brain of trauma victims. A systematic literature review on PubMed following PRISMA 2020 guidelines has enabled the identification of 241 articles. In all, 21 of these were enrolled to identify 24 markers that could be divided into two groups. The first consisted of well-known markers that could be considered for a first diagnosis of TBI. The second consisted of new markers recently proposed in the literature that could be used in combination with the markers of the first group to define the elapsed time between trauma and death. However, the use of these markers has to be validated in the future in human tissue by further studies, and the influence of other diseases affecting the victims before death should be explored. Full article
(This article belongs to the Special Issue Oxidative Stress and Brain Injury 3.0)
►▼ Show Figures

Figure 1

19 pages, 726 KiB  
Review
Oxidative Stress in Traumatic Brain Injury
by Arman Fesharaki-Zadeh
Int. J. Mol. Sci. 2022, 23(21), 13000; https://doi.org/10.3390/ijms232113000 - 27 Oct 2022
Cited by 30 | Viewed by 3329
Abstract
Traumatic Brain Injury (TBI) remains a major cause of disability worldwide. It involves a complex neurometabolic cascade, including oxidative stress. The products of this manuscript is examining the underlying pathophysiological mechanism, including reactive oxygen species (ROS) and reactive nitrogen species (RNS). This process [...] Read more.
Traumatic Brain Injury (TBI) remains a major cause of disability worldwide. It involves a complex neurometabolic cascade, including oxidative stress. The products of this manuscript is examining the underlying pathophysiological mechanism, including reactive oxygen species (ROS) and reactive nitrogen species (RNS). This process in turn leads to secondary injury cascade, which includes lipid peroxidation products. These reactions ultimately play a key role in chronic inflammation and synaptic dysfunction in a synergistic fashion. Although there are no FDA approved antioxidant therapy for TBI, there is a number of antioxidant therapies that have been tested and include free radical scavengers, activators of antioxidant systems, inhibitors of free radical generating enzymes, and antioxidant enzymes. Antioxidant therapies have led to cognitive and functional recovery post TBI, and they offer a promising treatment option for patients recovering from TBI. Current major challenges in treatment of TBI symptoms include heterogenous nature of injury, as well as access to timely treatment post injury. The inherent benefits of antioxidant therapies include minimally reported side effects, and relative ease of use in the clinical setting. The current review also provides a highlight of the more studied anti-oxidant regimen with applicability for TBI treatment with potential use in the real clinical setting. Full article
(This article belongs to the Special Issue Oxidative Stress and Brain Injury 3.0)
►▼ Show Figures

Graphical abstract

14 pages, 671 KiB  
Review
Glymphatic System a Window on TBI Pathophysiology: A Systematic Review
by Michela Ferrara, Giuseppe Bertozzi, Gianpietro Volonnino, Nicola Di Fazio, Paola Frati, Luigi Cipolloni, Raffaele La Russa and Vittorio Fineschi
Int. J. Mol. Sci. 2022, 23(16), 9138; https://doi.org/10.3390/ijms23169138 - 15 Aug 2022
Cited by 13 | Viewed by 2179
Abstract
Background: In recent years, the attention of the scientific world has focused on a clearance system of brain waste metabolites, called the glymphatic system, based on its similarity to the lymphatic system in peripheral tissue and the relevant role of the AQP4 glial [...] Read more.
Background: In recent years, the attention of the scientific world has focused on a clearance system of brain waste metabolites, called the glymphatic system, based on its similarity to the lymphatic system in peripheral tissue and the relevant role of the AQP4 glial channels and described for the first time in 2012. Consequently, numerous studies focused on its role in organ damage in cases of neuropathologies, including TBI. Methods: To evaluate the role that the glymphatic system has in the pathogenesis of TBI, on 23 March 2022, a systematic review of the literature according to PRISMA guidelines was carried out using the SCOPUS and Medline (via PubMed) databases, resulting in 12 articles after the selection process. Discussion and conclusion: The present review demonstrated that an alteration of AQP4 is associated with the accumulation of substances S100b, GFAP, and NSE, known markers of TBI in the forensic field. In addition, the alteration of the functionality of AQP4 favors edema, which, as already described, constitutes alterations of secondary brain injuries. Moreover, specific areas of the brain were demonstrated to be prone to alterations of the glymphatic pathway, suggesting their involvement in post-TBI damage. Therefore, further studies are mandatory. In this regard, a study protocol on cadavers is also proposed, based on the analyzed evidence. Full article
(This article belongs to the Special Issue Oxidative Stress and Brain Injury 3.0)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-5
Back to TopTop