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The role of selenium metabolism and selenoproteins in cartilage homeostasis and arthropathies

As an essential nutrient and trace element, selenium is required for living organisms and its beneficial roles in human health have been well recognized. The role of selenium is mainly played through selenoproteins synthesized by the selenium metabolic system. Selenoproteins have a wide range of cel...

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Autores principales: Kang, Donghyun, Lee, Jeeyeon, Wu, Cuiyan, Guo, Xiong, Lee, Byeong Jae, Chun, Jang-Soo, Kim, Jin-Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7423502/
https://www.ncbi.nlm.nih.gov/pubmed/32788658
http://dx.doi.org/10.1038/s12276-020-0408-y
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author Kang, Donghyun
Lee, Jeeyeon
Wu, Cuiyan
Guo, Xiong
Lee, Byeong Jae
Chun, Jang-Soo
Kim, Jin-Hong
author_facet Kang, Donghyun
Lee, Jeeyeon
Wu, Cuiyan
Guo, Xiong
Lee, Byeong Jae
Chun, Jang-Soo
Kim, Jin-Hong
author_sort Kang, Donghyun
collection PubMed
description As an essential nutrient and trace element, selenium is required for living organisms and its beneficial roles in human health have been well recognized. The role of selenium is mainly played through selenoproteins synthesized by the selenium metabolic system. Selenoproteins have a wide range of cellular functions including regulation of selenium transport, thyroid hormones, immunity, and redox homeostasis. Selenium deficiency contributes to various diseases, such as cardiovascular disease, cancer, liver disease, and arthropathy—Kashin–Beck disease (KBD) and osteoarthritis (OA). A skeletal developmental disorder, KBD has been reported in low-selenium areas of China, North Korea, and the Siberian region of Russia, and can be alleviated by selenium supplementation. OA, the most common form of arthritis, is a degenerative disease caused by an imbalance in matrix metabolism and is characterized by cartilage destruction. Oxidative stress serves as a major cause of the initiation of OA pathogenesis. Selenium deficiency and dysregulation of selenoproteins are associated with impairments to redox homeostasis in cartilage. We review the recently explored roles of selenium metabolism and selenoproteins in cartilage with an emphasis on two arthropathies, KBD and OA. Moreover, we discuss the potential of therapeutic strategies targeting the biological functions of selenium and selenoproteins for OA treatment.
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spelling pubmed-74235022020-08-13 The role of selenium metabolism and selenoproteins in cartilage homeostasis and arthropathies Kang, Donghyun Lee, Jeeyeon Wu, Cuiyan Guo, Xiong Lee, Byeong Jae Chun, Jang-Soo Kim, Jin-Hong Exp Mol Med Review Article As an essential nutrient and trace element, selenium is required for living organisms and its beneficial roles in human health have been well recognized. The role of selenium is mainly played through selenoproteins synthesized by the selenium metabolic system. Selenoproteins have a wide range of cellular functions including regulation of selenium transport, thyroid hormones, immunity, and redox homeostasis. Selenium deficiency contributes to various diseases, such as cardiovascular disease, cancer, liver disease, and arthropathy—Kashin–Beck disease (KBD) and osteoarthritis (OA). A skeletal developmental disorder, KBD has been reported in low-selenium areas of China, North Korea, and the Siberian region of Russia, and can be alleviated by selenium supplementation. OA, the most common form of arthritis, is a degenerative disease caused by an imbalance in matrix metabolism and is characterized by cartilage destruction. Oxidative stress serves as a major cause of the initiation of OA pathogenesis. Selenium deficiency and dysregulation of selenoproteins are associated with impairments to redox homeostasis in cartilage. We review the recently explored roles of selenium metabolism and selenoproteins in cartilage with an emphasis on two arthropathies, KBD and OA. Moreover, we discuss the potential of therapeutic strategies targeting the biological functions of selenium and selenoproteins for OA treatment. Nature Publishing Group UK 2020-08-13 /pmc/articles/PMC7423502/ /pubmed/32788658 http://dx.doi.org/10.1038/s12276-020-0408-y Text en © The Author(s) 2020 https://creativecommons.org/licenses/by/4.0/Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Review Article
Kang, Donghyun
Lee, Jeeyeon
Wu, Cuiyan
Guo, Xiong
Lee, Byeong Jae
Chun, Jang-Soo
Kim, Jin-Hong
The role of selenium metabolism and selenoproteins in cartilage homeostasis and arthropathies
title The role of selenium metabolism and selenoproteins in cartilage homeostasis and arthropathies
title_full The role of selenium metabolism and selenoproteins in cartilage homeostasis and arthropathies
title_fullStr The role of selenium metabolism and selenoproteins in cartilage homeostasis and arthropathies
title_full_unstemmed The role of selenium metabolism and selenoproteins in cartilage homeostasis and arthropathies
title_short The role of selenium metabolism and selenoproteins in cartilage homeostasis and arthropathies
title_sort role of selenium metabolism and selenoproteins in cartilage homeostasis and arthropathies
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7423502/
https://www.ncbi.nlm.nih.gov/pubmed/32788658
http://dx.doi.org/10.1038/s12276-020-0408-y
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