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Drivers of phenotypic variation in cartilage: Circadian clock genes

Endogenous homeostasis and peripheral tissue metabolism are disrupted by irregular fluctuations in activation, movement, feeding and temperature, which can accelerate negative biological processes and lead to immune reactions, such as rheumatoid arthritis (RA) and osteoarthritis (OA). This review su...

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Detalles Bibliográficos
Autores principales: Song, Xiaopeng, Bai, Hui, Meng, Xinghua, Xiao, Jianhua, Gao, Li
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8358851/
https://www.ncbi.nlm.nih.gov/pubmed/34213828
http://dx.doi.org/10.1111/jcmm.16768
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author Song, Xiaopeng
Bai, Hui
Meng, Xinghua
Xiao, Jianhua
Gao, Li
author_facet Song, Xiaopeng
Bai, Hui
Meng, Xinghua
Xiao, Jianhua
Gao, Li
author_sort Song, Xiaopeng
collection PubMed
description Endogenous homeostasis and peripheral tissue metabolism are disrupted by irregular fluctuations in activation, movement, feeding and temperature, which can accelerate negative biological processes and lead to immune reactions, such as rheumatoid arthritis (RA) and osteoarthritis (OA). This review summarizes abnormal phenotypes in articular joint components such as cartilage, bone and the synovium, attributed to the deletion or overexpression of clock genes in cartilage or chondrocytes. Understanding the functional mechanisms of different genes, the differentiation of mouse phenotypes and the prevention of joint ageing and disease will facilitate future research.
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spelling pubmed-83588512021-08-15 Drivers of phenotypic variation in cartilage: Circadian clock genes Song, Xiaopeng Bai, Hui Meng, Xinghua Xiao, Jianhua Gao, Li J Cell Mol Med Reviews Endogenous homeostasis and peripheral tissue metabolism are disrupted by irregular fluctuations in activation, movement, feeding and temperature, which can accelerate negative biological processes and lead to immune reactions, such as rheumatoid arthritis (RA) and osteoarthritis (OA). This review summarizes abnormal phenotypes in articular joint components such as cartilage, bone and the synovium, attributed to the deletion or overexpression of clock genes in cartilage or chondrocytes. Understanding the functional mechanisms of different genes, the differentiation of mouse phenotypes and the prevention of joint ageing and disease will facilitate future research. John Wiley and Sons Inc. 2021-07-02 2021-08 /pmc/articles/PMC8358851/ /pubmed/34213828 http://dx.doi.org/10.1111/jcmm.16768 Text en © 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Reviews
Song, Xiaopeng
Bai, Hui
Meng, Xinghua
Xiao, Jianhua
Gao, Li
Drivers of phenotypic variation in cartilage: Circadian clock genes
title Drivers of phenotypic variation in cartilage: Circadian clock genes
title_full Drivers of phenotypic variation in cartilage: Circadian clock genes
title_fullStr Drivers of phenotypic variation in cartilage: Circadian clock genes
title_full_unstemmed Drivers of phenotypic variation in cartilage: Circadian clock genes
title_short Drivers of phenotypic variation in cartilage: Circadian clock genes
title_sort drivers of phenotypic variation in cartilage: circadian clock genes
topic Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8358851/
https://www.ncbi.nlm.nih.gov/pubmed/34213828
http://dx.doi.org/10.1111/jcmm.16768
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