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Role of NADPH Oxidases in Blood–Brain Barrier Disruption and Ischemic Stroke
NADPH oxidases (Nox) are one of the main sources of reactive oxygen species (ROS) in the central nervous system (CNS). While these enzymes have been shown to be involved in physiological regulation of cerebral vascular tone, excessive ROS produced by Nox1-5 play a critical role in blood–brain barrie...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9598888/ https://www.ncbi.nlm.nih.gov/pubmed/36290688 http://dx.doi.org/10.3390/antiox11101966 |
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author | Hernandes, Marina S. Xu, Qian Griendling, Kathy K. |
author_facet | Hernandes, Marina S. Xu, Qian Griendling, Kathy K. |
author_sort | Hernandes, Marina S. |
collection | PubMed |
description | NADPH oxidases (Nox) are one of the main sources of reactive oxygen species (ROS) in the central nervous system (CNS). While these enzymes have been shown to be involved in physiological regulation of cerebral vascular tone, excessive ROS produced by Nox1-5 play a critical role in blood–brain barrier (BBB) dysfunction in numerous neuropathologies. Nox-derived ROS have been implicated in mediating matrix metalloprotease (MMP) activation, downregulation of junctional complexes between adjacent brain endothelial cells and brain endothelial cell apoptosis, leading to brain microvascular endothelial barrier dysfunction and consequently, increases in BBB permeability. In this review, we will highlight recent findings on the role played by these enzymes in BBB disruption induced by ischemic stroke. |
format | Online Article Text |
id | pubmed-9598888 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-95988882022-10-27 Role of NADPH Oxidases in Blood–Brain Barrier Disruption and Ischemic Stroke Hernandes, Marina S. Xu, Qian Griendling, Kathy K. Antioxidants (Basel) Review NADPH oxidases (Nox) are one of the main sources of reactive oxygen species (ROS) in the central nervous system (CNS). While these enzymes have been shown to be involved in physiological regulation of cerebral vascular tone, excessive ROS produced by Nox1-5 play a critical role in blood–brain barrier (BBB) dysfunction in numerous neuropathologies. Nox-derived ROS have been implicated in mediating matrix metalloprotease (MMP) activation, downregulation of junctional complexes between adjacent brain endothelial cells and brain endothelial cell apoptosis, leading to brain microvascular endothelial barrier dysfunction and consequently, increases in BBB permeability. In this review, we will highlight recent findings on the role played by these enzymes in BBB disruption induced by ischemic stroke. MDPI 2022-09-30 /pmc/articles/PMC9598888/ /pubmed/36290688 http://dx.doi.org/10.3390/antiox11101966 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 Hernandes, Marina S. Xu, Qian Griendling, Kathy K. Role of NADPH Oxidases in Blood–Brain Barrier Disruption and Ischemic Stroke |
title | Role of NADPH Oxidases in Blood–Brain Barrier Disruption and Ischemic Stroke |
title_full | Role of NADPH Oxidases in Blood–Brain Barrier Disruption and Ischemic Stroke |
title_fullStr | Role of NADPH Oxidases in Blood–Brain Barrier Disruption and Ischemic Stroke |
title_full_unstemmed | Role of NADPH Oxidases in Blood–Brain Barrier Disruption and Ischemic Stroke |
title_short | Role of NADPH Oxidases in Blood–Brain Barrier Disruption and Ischemic Stroke |
title_sort | role of nadph oxidases in blood–brain barrier disruption and ischemic stroke |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9598888/ https://www.ncbi.nlm.nih.gov/pubmed/36290688 http://dx.doi.org/10.3390/antiox11101966 |
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