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Pathophysiological implications of hypoxia in human diseases

Oxygen is essentially required by most eukaryotic organisms as a scavenger to remove harmful electron and hydrogen ions or as a critical substrate to ensure the proper execution of enzymatic reactions. All nucleated cells can sense oxygen concentration and respond to reduced oxygen availability (hyp...

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Autores principales: Chen, Pai-Sheng, Chiu, Wen-Tai, Hsu, Pei-Ling, Lin, Shih-Chieh, Peng, I-Chen, Wang, Chia-Yih, Tsai, Shaw-Jenq
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7212687/
https://www.ncbi.nlm.nih.gov/pubmed/32389123
http://dx.doi.org/10.1186/s12929-020-00658-7
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author Chen, Pai-Sheng
Chiu, Wen-Tai
Hsu, Pei-Ling
Lin, Shih-Chieh
Peng, I-Chen
Wang, Chia-Yih
Tsai, Shaw-Jenq
author_facet Chen, Pai-Sheng
Chiu, Wen-Tai
Hsu, Pei-Ling
Lin, Shih-Chieh
Peng, I-Chen
Wang, Chia-Yih
Tsai, Shaw-Jenq
author_sort Chen, Pai-Sheng
collection PubMed
description Oxygen is essentially required by most eukaryotic organisms as a scavenger to remove harmful electron and hydrogen ions or as a critical substrate to ensure the proper execution of enzymatic reactions. All nucleated cells can sense oxygen concentration and respond to reduced oxygen availability (hypoxia). When oxygen delivery is disrupted or reduced, the organisms will develop numerous adaptive mechanisms to facilitate cells survived in the hypoxic condition. Normally, such hypoxic response will cease when oxygen level is restored. However, the situation becomes complicated if hypoxic stress persists (chronic hypoxia) or cyclic normoxia-hypoxia phenomenon occurs (intermittent hypoxia). A series of chain reaction-like gene expression cascade, termed hypoxia-mediated gene regulatory network, will be initiated under such prolonged or intermittent hypoxic conditions and subsequently leads to alteration of cellular function and/or behaviors. As a result, irreversible processes occur that may cause physiological disorder or even pathological consequences. A growing body of evidence implicates that hypoxia plays critical roles in the pathogenesis of major causes of mortality including cancer, myocardial ischemia, metabolic diseases, and chronic heart and kidney diseases, and in reproductive diseases such as preeclampsia and endometriosis. This review article will summarize current understandings regarding the molecular mechanism of hypoxia in these common and important diseases.
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spelling pubmed-72126872020-05-18 Pathophysiological implications of hypoxia in human diseases Chen, Pai-Sheng Chiu, Wen-Tai Hsu, Pei-Ling Lin, Shih-Chieh Peng, I-Chen Wang, Chia-Yih Tsai, Shaw-Jenq J Biomed Sci Review Oxygen is essentially required by most eukaryotic organisms as a scavenger to remove harmful electron and hydrogen ions or as a critical substrate to ensure the proper execution of enzymatic reactions. All nucleated cells can sense oxygen concentration and respond to reduced oxygen availability (hypoxia). When oxygen delivery is disrupted or reduced, the organisms will develop numerous adaptive mechanisms to facilitate cells survived in the hypoxic condition. Normally, such hypoxic response will cease when oxygen level is restored. However, the situation becomes complicated if hypoxic stress persists (chronic hypoxia) or cyclic normoxia-hypoxia phenomenon occurs (intermittent hypoxia). A series of chain reaction-like gene expression cascade, termed hypoxia-mediated gene regulatory network, will be initiated under such prolonged or intermittent hypoxic conditions and subsequently leads to alteration of cellular function and/or behaviors. As a result, irreversible processes occur that may cause physiological disorder or even pathological consequences. A growing body of evidence implicates that hypoxia plays critical roles in the pathogenesis of major causes of mortality including cancer, myocardial ischemia, metabolic diseases, and chronic heart and kidney diseases, and in reproductive diseases such as preeclampsia and endometriosis. This review article will summarize current understandings regarding the molecular mechanism of hypoxia in these common and important diseases. BioMed Central 2020-05-11 /pmc/articles/PMC7212687/ /pubmed/32389123 http://dx.doi.org/10.1186/s12929-020-00658-7 Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.
spellingShingle Review
Chen, Pai-Sheng
Chiu, Wen-Tai
Hsu, Pei-Ling
Lin, Shih-Chieh
Peng, I-Chen
Wang, Chia-Yih
Tsai, Shaw-Jenq
Pathophysiological implications of hypoxia in human diseases
title Pathophysiological implications of hypoxia in human diseases
title_full Pathophysiological implications of hypoxia in human diseases
title_fullStr Pathophysiological implications of hypoxia in human diseases
title_full_unstemmed Pathophysiological implications of hypoxia in human diseases
title_short Pathophysiological implications of hypoxia in human diseases
title_sort pathophysiological implications of hypoxia in human diseases
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7212687/
https://www.ncbi.nlm.nih.gov/pubmed/32389123
http://dx.doi.org/10.1186/s12929-020-00658-7
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