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Mitochondrial complex II and reactive oxygen species in disease and therapy
Increasing evidence points to the respiratory Complex II (CII) as a source and modulator of reactive oxygen species (ROS). Both functional loss of CII as well as its pharmacological inhibition can lead to ROS generation in cells, with a relevant impact on the development of pathophysiological condit...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7178880/ https://www.ncbi.nlm.nih.gov/pubmed/32290794 http://dx.doi.org/10.1080/13510002.2020.1752002 |
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author | Hadrava Vanova, Katerina Kraus, Michal Neuzil, Jiri Rohlena, Jakub |
author_facet | Hadrava Vanova, Katerina Kraus, Michal Neuzil, Jiri Rohlena, Jakub |
author_sort | Hadrava Vanova, Katerina |
collection | PubMed |
description | Increasing evidence points to the respiratory Complex II (CII) as a source and modulator of reactive oxygen species (ROS). Both functional loss of CII as well as its pharmacological inhibition can lead to ROS generation in cells, with a relevant impact on the development of pathophysiological conditions, i.e. cancer and neurodegenerative diseases. While the basic framework of CII involvement in ROS production has been defined, the fine details still await clarification. It is important to resolve these aspects to fully understand the role of CII in pathology and to explore its therapeutic potential in cancer and other diseases. |
format | Online Article Text |
id | pubmed-7178880 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-71788802020-05-01 Mitochondrial complex II and reactive oxygen species in disease and therapy Hadrava Vanova, Katerina Kraus, Michal Neuzil, Jiri Rohlena, Jakub Redox Rep Review Article Increasing evidence points to the respiratory Complex II (CII) as a source and modulator of reactive oxygen species (ROS). Both functional loss of CII as well as its pharmacological inhibition can lead to ROS generation in cells, with a relevant impact on the development of pathophysiological conditions, i.e. cancer and neurodegenerative diseases. While the basic framework of CII involvement in ROS production has been defined, the fine details still await clarification. It is important to resolve these aspects to fully understand the role of CII in pathology and to explore its therapeutic potential in cancer and other diseases. Taylor & Francis 2020-04-14 /pmc/articles/PMC7178880/ /pubmed/32290794 http://dx.doi.org/10.1080/13510002.2020.1752002 Text en © 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Hadrava Vanova, Katerina Kraus, Michal Neuzil, Jiri Rohlena, Jakub Mitochondrial complex II and reactive oxygen species in disease and therapy |
title | Mitochondrial complex II and reactive oxygen species in disease and therapy |
title_full | Mitochondrial complex II and reactive oxygen species in disease and therapy |
title_fullStr | Mitochondrial complex II and reactive oxygen species in disease and therapy |
title_full_unstemmed | Mitochondrial complex II and reactive oxygen species in disease and therapy |
title_short | Mitochondrial complex II and reactive oxygen species in disease and therapy |
title_sort | mitochondrial complex ii and reactive oxygen species in disease and therapy |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7178880/ https://www.ncbi.nlm.nih.gov/pubmed/32290794 http://dx.doi.org/10.1080/13510002.2020.1752002 |
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