Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.8
7.0
Journals
Antioxidants
Special Issues
Oxidative Stress and Its Role in Ischemic Stroke
share announcement

Oxidative Stress and Its Role in Ischemic Stroke

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 5961

Special Issue Editors

Dr. Syed Shadab Raza

E-Mail Website
Guest Editor
Department of Stem Cell Biology and Regenerative Medicine, Era’s Lucknow Medical College & Hospital, Era University, Lucknow 226003, India
Interests: ischemic stroke; stem cell transplantation; neurogenesis; oxidative Stress; inflammation; nanomedicine
Prof. Dr. Johannes Boltze

E-Mail Website
Guest Editor
Department of Life Sciences, University of Warwick, Coventry CV4 7AL, UK
Interests: ischemic stroke; cerebrovascular disease; cell therapies; neuroprotection; translational research

Special Issue Information

Dear Colleagues,

Stroke is the third leading cause of death and the leading cause of long-term disability worldwide. Stroke imposes a significant socioeconomic burden, emphasizing the critical need for effective treatments. The World Health Organization (WHO) estimates that 15 million people have strokes each year. Over 6 million of these people die and another 5 million are permanently disabled. Currently available treatments for acute ischemic stroke include intravenous tissue plasminogen activator (tPA) administration and endovascular treatment.

However, these treatments have the disadvantage of exposing the brain to extremely harmful reactive oxygen species (ROS) during recanalization. This results in oxidative stress being a major cause of ischemia-reperfusion injuries and, thus, secondary brain tissue damage. Oxidative stress causes damage to proteins, lipids, and DNA due to an imbalance between ROS production and the antioxidant system that could lead to apoptosis, autophagy, and necrosis in brain cells. As a result, it is critical to comprehend the mechanisms driving the production of reactive oxygen species (ROS), their function in the pathophysiology of ischemic stroke, and current advances in treatment techniques for lowering oxidative stress following ischemic stroke. To combat the impact of oxidative stress during ischemic stroke, pharmacological intervention with antioxidants or boosters of endogenous antioxidant molecules may be an ideal approach. Moreover, the impact of oxidative stress on emerging experimental therapeutics needs to be understood.

The goal of this Special Issue of Antioxidants is to bring together new data and interpretations on all aspects of ischemic brain function in relation to ROS. Contributions on the role of ROS at the cellular level, as well as novel findings on ischemic stroke and related brain disorders in relation to oxidative stress, are encouraged. We also welcome submissions reporting therapeutic approaches that utilize endogenous antioxidant pathways and exogenous antioxidants to reverse the negative effects of oxidative stress in ischemic brains. 

Dr. Syed Shadab Raza
Prof. Dr. Johannes Boltze
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. Antioxidants 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 2900 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

  • ischemic stroke
  • transient ischemic attack
  • cerebrovascular disease
  • oxidative stress
  • free radicals
  • reactive oxygen species
  • reactive nitrogen species
  • pathophysiology
  • neuronal cell death
  • neuroprotection
  • recanalization
  • antioxidant therapy
  • cell therapy
  • translational research

Published Papers (4 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

23 pages, 11941 KiB  
Article
Neuroprotection Afforded by an Enriched Mediterranean-like Diet Is Modified by Exercise in a Rat Male Model of Cerebral Ischemia
by Daniel Romaus-Sanjurjo, María Castañón-Apilánez, Esteban López-Arias, Antía Custodia, Cristina Martin-Martín, Alberto Ouro, Elena López-Cancio and Tomás Sobrino
Antioxidants 2024, 13(2), 138; https://doi.org/10.3390/antiox13020138 - 23 Jan 2024
Viewed by 1040
Abstract
Ischemic stroke is an important cause of mortality and disability worldwide. Given that current treatments do not allow a remarkably better outcome in patients after stroke, it is mandatory to seek new approaches to preventing stroke and/or complementing the current treatments or ameliorating [...] Read more.
Ischemic stroke is an important cause of mortality and disability worldwide. Given that current treatments do not allow a remarkably better outcome in patients after stroke, it is mandatory to seek new approaches to preventing stroke and/or complementing the current treatments or ameliorating the ischemic insult. Multiple preclinical and clinical studies highlighted the potential beneficial roles of exercise and a Mediterranean diet following a stroke. Here, we investigated the effects of a pre-stroke Mediterranean-like diet supplemented with hydroxytyrosol and with/without physical exercise on male rats undergoing transient middle cerebral artery occlusion (tMCAO). We also assessed a potential synergistic effect with physical exercise. Our findings indicated that the diet reduced infarct and edema volumes, modulated acute immune response by altering cytokine and chemokine levels, decreased oxidative stress, and improved acute functional recovery post-ischemic injury. Interestingly, while physical exercise alone improved certain outcomes compared to control animals, it did not enhance, and in some aspects even impaired, the positive effects of the Mediterranean-like diet in the short term. Overall, these data provide the first preclinical evidence that a preemptive enriched Mediterranean diet modulates cytokines/chemokines levels downwards which eventually has an important role during the acute phase following ischemic damage, likely mediating neuroprotection. Full article
(This article belongs to the Special Issue Oxidative Stress and Its Role in Ischemic Stroke)
►▼ Show Figures

Figure 1

16 pages, 3708 KiB  
Article
A Metabolomic Signature of Ischemic Stroke Showing Acute Oxidative and Energetic Stress
by Moustapha Djite, Juan Manuel Chao de la Barca, Cinzia Bocca, Ndiaga Matar Gaye, Néné Oumou Kesso Barry, Mame Ndoumbé Mbacke, Ousmane Cissé, Pape Matar Kandji, Ndèye Marème Thioune, Najah Fatou Coly-Gueye, El Hadji Malick Ndour, Fatou Gueye-Tall, Amadou Gallo Diop, Gilles Simard, Delphine Mirebeau-Prunier, Papa Madieye Gueye and Pascal Reynier
Antioxidants 2024, 13(1), 60; https://doi.org/10.3390/antiox13010060 - 29 Dec 2023
Viewed by 963
Abstract
Metabolomics is a powerful data-driven tool for in-depth biological phenotyping that could help identify the specific metabolic profile of cryptogenic strokes, for which no precise cause has been identified. We performed a targeted quantitative metabolomics study in West African patients who had recently [...] Read more.
Metabolomics is a powerful data-driven tool for in-depth biological phenotyping that could help identify the specific metabolic profile of cryptogenic strokes, for which no precise cause has been identified. We performed a targeted quantitative metabolomics study in West African patients who had recently suffered an ischemic stroke, which was either cryptogenic (n = 40) or had a clearly identified cause (n = 39), compared to a healthy control group (n = 40). Four hundred fifty-six metabolites were accurately measured. Multivariate analyses failed to reveal any metabolic profile discriminating between cryptogenic ischemic strokes and those with an identified cause but did show superimposable metabolic profiles in both groups, which were clearly distinct from those of healthy controls. The blood concentrations of 234 metabolites were significantly affected in stroke patients compared to controls after the Benjamini–Hochberg correction. Increased methionine sulfoxide and homocysteine concentrations, as well as an overall increase in saturation of fatty acids, were indicative of acute oxidative stress. This signature also showed alterations in energetic metabolism, cell membrane integrity, monocarbon metabolism, and neurotransmission, with reduced concentrations of several metabolites known to be neuroprotective. Overall, our results show that cryptogenic strokes are not pathophysiologically distinct from ischemic strokes of established origin, and that stroke leads to intense metabolic remodeling with marked oxidative and energetic stresses. Full article
(This article belongs to the Special Issue Oxidative Stress and Its Role in Ischemic Stroke)
►▼ Show Figures

Figure 1

18 pages, 4058 KiB  
Article
Targeting Pro-Oxidant Iron with Exogenously Administered Apotransferrin Provides Benefits Associated with Changes in Crucial Cellular Iron Gate Protein TfR in a Model of Intracerebral Hemorrhagic Stroke in Mice
by Alexia García-Serran, Jesús Ordoño, Núria DeGregorio-Rocasolano, Marc Melià-Sorolla, Karla Odendaal, Octavi Martí-Sistac and Teresa Gasull
Antioxidants 2023, 12(11), 1945; https://doi.org/10.3390/antiox12111945 - 31 Oct 2023
Viewed by 1271
Abstract
We have previously demonstrated that the post-stroke administration of iron-free transferrin (apotransferrin, ATf) is beneficial in different models of ischemic stroke (IS) through the inhibition of the neuronal uptake of pro-oxidant iron. In the present study, we asked whether ATf is safe and [...] Read more.
We have previously demonstrated that the post-stroke administration of iron-free transferrin (apotransferrin, ATf) is beneficial in different models of ischemic stroke (IS) through the inhibition of the neuronal uptake of pro-oxidant iron. In the present study, we asked whether ATf is safe and also beneficial when given after the induction of intracerebral hemorrhage (ICH) in mice, and investigated the underlying mechanisms. We first compared the main iron actors in the brain of IS- or collagenase-induced ICH mice and then obtained insight into these iron-related proteins in ICH 72 h after the administration of ATf. The infarct size of the IS mice was double that of hemorrhage in ICH mice, but both groups showed similar body weight loss, edema, and increased ferritin and transferrin levels in the ipsilateral brain hemisphere. Although the administration of human ATf (hATf) to ICH mice did not alter the hemorrhage volume or levels of the classical ferroptosis GPX4/system xc- pathways, hATf induced better neurobehavioral performance, decreased 4-hydroxynonenal levels and those of the second-generation ferroptosis marker transferrin receptor (TfR), and restored the mRNA levels of the recently recognized cytosolic iron chaperone poly(RC) binding protein 2. In addition, hATf treatment lowered the ICH-induced increase in both endogenous mouse transferrin mRNA levels and the activation of caspase-2. In conclusion, hATf treatment provides neurobehavioral benefits post-ICH associated with the modulation of iron/oxidative players. Full article
(This article belongs to the Special Issue Oxidative Stress and Its Role in Ischemic Stroke)
►▼ Show Figures

Figure 1

25 pages, 3292 KiB  
Article
An Electrophysiological and Proteomic Analysis of the Effects of the Superoxide Dismutase Mimetic, MnTMPyP, on Synaptic Signalling Post-Ischemia in Isolated Rat Hippocampal Slices
by Martina Puzio, Niamh Moreton, Mairéad Sullivan, Caitriona Scaife, Jeffrey C. Glennon and John J. O’Connor
Antioxidants 2023, 12(4), 792; https://doi.org/10.3390/antiox12040792 - 24 Mar 2023
Cited by 1 | Viewed by 1883
Abstract
Metabolic stress and the increased production of reactive oxygen species (ROS) are two main contributors to neuronal damage and synaptic plasticity in acute ischemic stroke. The superoxide scavenger MnTMPyP has been previously reported to have a neuroprotective effect in organotypic hippocampal slices and [...] Read more.
Metabolic stress and the increased production of reactive oxygen species (ROS) are two main contributors to neuronal damage and synaptic plasticity in acute ischemic stroke. The superoxide scavenger MnTMPyP has been previously reported to have a neuroprotective effect in organotypic hippocampal slices and to modulate synaptic transmission after in vitro hypoxia and oxygen–glucose deprivation (OGD). However, the mechanisms involved in the effect of this scavenger remain elusive. In this study, two concentrations of MnTMPyP were evaluated on synaptic transmission during ischemia and post-ischemic synaptic potentiation. The complex molecular changes supporting cellular adaptation to metabolic stress, and how these are modulated by MnTMPyP, were also investigated. Electrophysiological data showed that MnTMPyP causes a decrease in baseline synaptic transmission and impairment of synaptic potentiation. Proteomic analysis performed on MnTMPyP and hypoxia-treated tissue indicated an impairment in vesicular trafficking mechanisms, including reduced expression of Hsp90 and actin signalling. Alterations of vesicular trafficking may lead to reduced probability of neurotransmitter release and AMPA receptor activity, resulting in the observed modulatory effect of MnTMPyP. In OGD, protein enrichment analysis highlighted impairments in cell proliferation and differentiation, such as TGFβ1 and CDKN1B signalling, in addition to downregulation of mitochondrial dysfunction and an increased expression of CAMKII. Taken together, our results may indicate modulation of neuronal sensitivity to the ischemic insult, and a complex role for MnTMPyP in synaptic transmission and plasticity, potentially providing molecular insights into the mechanisms mediating the effects of MnTMPyP during ischemia. Full article
(This article belongs to the Special Issue Oxidative Stress and Its Role in Ischemic Stroke)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop