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Hypoxia and its implications in rheumatoid arthritis

Alterations in tissue oxygen pressure contribute to a number of diseases, including rheumatoid arthritis (RA). Low partial pressure of oxygen, a condition known as hypoxia, is a relevant feature in RA since it is involved in angiogenesis, inflammation, apoptosis, cartilage degradation, energy metabo...

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Autores principales: Quiñonez-Flores, Celia María, González-Chávez, Susana Aideé, Pacheco-Tena, César
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4994473/
https://www.ncbi.nlm.nih.gov/pubmed/27549205
http://dx.doi.org/10.1186/s12929-016-0281-0
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author Quiñonez-Flores, Celia María
González-Chávez, Susana Aideé
Pacheco-Tena, César
author_facet Quiñonez-Flores, Celia María
González-Chávez, Susana Aideé
Pacheco-Tena, César
author_sort Quiñonez-Flores, Celia María
collection PubMed
description Alterations in tissue oxygen pressure contribute to a number of diseases, including rheumatoid arthritis (RA). Low partial pressure of oxygen, a condition known as hypoxia, is a relevant feature in RA since it is involved in angiogenesis, inflammation, apoptosis, cartilage degradation, energy metabolism, and oxidative damage. Therefore, alterations in hypoxia-related signaling pathways are considered potential mechanisms of disease pathogenesis. The objective of this review is to highlight and update our current knowledge of the role of hypoxia in the pathogenesis of RA. We describe the experimental evidence that RA synovial tissue exists in a hypoxic state, as well as the origin and involvement of synovial hypoxia in different aspects of the pathogenic process.
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spelling pubmed-49944732016-08-24 Hypoxia and its implications in rheumatoid arthritis Quiñonez-Flores, Celia María González-Chávez, Susana Aideé Pacheco-Tena, César J Biomed Sci Review Alterations in tissue oxygen pressure contribute to a number of diseases, including rheumatoid arthritis (RA). Low partial pressure of oxygen, a condition known as hypoxia, is a relevant feature in RA since it is involved in angiogenesis, inflammation, apoptosis, cartilage degradation, energy metabolism, and oxidative damage. Therefore, alterations in hypoxia-related signaling pathways are considered potential mechanisms of disease pathogenesis. The objective of this review is to highlight and update our current knowledge of the role of hypoxia in the pathogenesis of RA. We describe the experimental evidence that RA synovial tissue exists in a hypoxic state, as well as the origin and involvement of synovial hypoxia in different aspects of the pathogenic process. BioMed Central 2016-08-22 /pmc/articles/PMC4994473/ /pubmed/27549205 http://dx.doi.org/10.1186/s12929-016-0281-0 Text en © The Author(s). 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Quiñonez-Flores, Celia María
González-Chávez, Susana Aideé
Pacheco-Tena, César
Hypoxia and its implications in rheumatoid arthritis
title Hypoxia and its implications in rheumatoid arthritis
title_full Hypoxia and its implications in rheumatoid arthritis
title_fullStr Hypoxia and its implications in rheumatoid arthritis
title_full_unstemmed Hypoxia and its implications in rheumatoid arthritis
title_short Hypoxia and its implications in rheumatoid arthritis
title_sort hypoxia and its implications in rheumatoid arthritis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4994473/
https://www.ncbi.nlm.nih.gov/pubmed/27549205
http://dx.doi.org/10.1186/s12929-016-0281-0
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