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Oxidative Stress in Ischemia/Reperfusion Injuries following Acute Ischemic Stroke

Recanalization therapy is increasingly used in the treatment of acute ischemic stroke. However, in about one third of these patients, recanalization is followed by ischemia/reperfusion injuries, and clinically to worsening of the neurological status. Much research has focused on unraveling the invol...

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Detalles Bibliográficos
Autores principales: Jurcau, Anamaria, Ardelean, Adriana Ioana
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8945353/
https://www.ncbi.nlm.nih.gov/pubmed/35327376
http://dx.doi.org/10.3390/biomedicines10030574
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author Jurcau, Anamaria
Ardelean, Adriana Ioana
author_facet Jurcau, Anamaria
Ardelean, Adriana Ioana
author_sort Jurcau, Anamaria
collection PubMed
description Recanalization therapy is increasingly used in the treatment of acute ischemic stroke. However, in about one third of these patients, recanalization is followed by ischemia/reperfusion injuries, and clinically to worsening of the neurological status. Much research has focused on unraveling the involved mechanisms in order to prevent or efficiently treat these injuries. What we know so far is that oxidative stress and mitochondrial dysfunction are significantly involved in the pathogenesis of ischemia/reperfusion injury. However, despite promising results obtained in experimental research, clinical studies trying to interfere with the oxidative pathways have mostly failed. The current article discusses the main mechanisms leading to ischemia/reperfusion injuries, such as mitochondrial dysfunction, excitotoxicity, and oxidative stress, and reviews the clinical trials with antioxidant molecules highlighting recent developments and future strategies.
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spelling pubmed-89453532022-03-25 Oxidative Stress in Ischemia/Reperfusion Injuries following Acute Ischemic Stroke Jurcau, Anamaria Ardelean, Adriana Ioana Biomedicines Review Recanalization therapy is increasingly used in the treatment of acute ischemic stroke. However, in about one third of these patients, recanalization is followed by ischemia/reperfusion injuries, and clinically to worsening of the neurological status. Much research has focused on unraveling the involved mechanisms in order to prevent or efficiently treat these injuries. What we know so far is that oxidative stress and mitochondrial dysfunction are significantly involved in the pathogenesis of ischemia/reperfusion injury. However, despite promising results obtained in experimental research, clinical studies trying to interfere with the oxidative pathways have mostly failed. The current article discusses the main mechanisms leading to ischemia/reperfusion injuries, such as mitochondrial dysfunction, excitotoxicity, and oxidative stress, and reviews the clinical trials with antioxidant molecules highlighting recent developments and future strategies. MDPI 2022-03-01 /pmc/articles/PMC8945353/ /pubmed/35327376 http://dx.doi.org/10.3390/biomedicines10030574 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Jurcau, Anamaria
Ardelean, Adriana Ioana
Oxidative Stress in Ischemia/Reperfusion Injuries following Acute Ischemic Stroke
title Oxidative Stress in Ischemia/Reperfusion Injuries following Acute Ischemic Stroke
title_full Oxidative Stress in Ischemia/Reperfusion Injuries following Acute Ischemic Stroke
title_fullStr Oxidative Stress in Ischemia/Reperfusion Injuries following Acute Ischemic Stroke
title_full_unstemmed Oxidative Stress in Ischemia/Reperfusion Injuries following Acute Ischemic Stroke
title_short Oxidative Stress in Ischemia/Reperfusion Injuries following Acute Ischemic Stroke
title_sort oxidative stress in ischemia/reperfusion injuries following acute ischemic stroke
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8945353/
https://www.ncbi.nlm.nih.gov/pubmed/35327376
http://dx.doi.org/10.3390/biomedicines10030574
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