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Ageing and osteoarthritis: a circadian rhythm connection

Osteoarthritis (OA) is the most common joint disease, affecting articular cartilage of the joints, with currently no cure. Age is a major risk factor for OA, but despite significant advances made in the OA research field, how ageing contributes to OA is still not well understood. In this review, we...

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Detalles Bibliográficos
Autores principales: Gossan, Nicole, Boot-Handford, Ray, Meng, Qing-Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Netherlands 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4361727/
https://www.ncbi.nlm.nih.gov/pubmed/25078075
http://dx.doi.org/10.1007/s10522-014-9522-3
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author Gossan, Nicole
Boot-Handford, Ray
Meng, Qing-Jun
author_facet Gossan, Nicole
Boot-Handford, Ray
Meng, Qing-Jun
author_sort Gossan, Nicole
collection PubMed
description Osteoarthritis (OA) is the most common joint disease, affecting articular cartilage of the joints, with currently no cure. Age is a major risk factor for OA, but despite significant advances made in the OA research field, how ageing contributes to OA is still not well understood. In this review, we will focus on one particular aspect of chondrocyte biology, i.e., circadian rhythms. Disruptions to circadian clocks have been linked to various diseases. Our recent work demonstrates autonomous clocks in chondrocytes which regulate key pathways implicated in OA. The cartilage rhythm dampens with age and clock gene expression changes during the initiation stage of OA development in an experimental mouse OA model. Research into the molecular links between ageing, circadian clocks and OA may identify novel therapeutic routes for the prevention and management of OA, such as chronotherapy, or direct targeting of clock components/circadian rhythm.
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spelling pubmed-43617272015-03-20 Ageing and osteoarthritis: a circadian rhythm connection Gossan, Nicole Boot-Handford, Ray Meng, Qing-Jun Biogerontology Review Article Osteoarthritis (OA) is the most common joint disease, affecting articular cartilage of the joints, with currently no cure. Age is a major risk factor for OA, but despite significant advances made in the OA research field, how ageing contributes to OA is still not well understood. In this review, we will focus on one particular aspect of chondrocyte biology, i.e., circadian rhythms. Disruptions to circadian clocks have been linked to various diseases. Our recent work demonstrates autonomous clocks in chondrocytes which regulate key pathways implicated in OA. The cartilage rhythm dampens with age and clock gene expression changes during the initiation stage of OA development in an experimental mouse OA model. Research into the molecular links between ageing, circadian clocks and OA may identify novel therapeutic routes for the prevention and management of OA, such as chronotherapy, or direct targeting of clock components/circadian rhythm. Springer Netherlands 2014-07-31 2015 /pmc/articles/PMC4361727/ /pubmed/25078075 http://dx.doi.org/10.1007/s10522-014-9522-3 Text en © The Author(s) 2014 https://creativecommons.org/licenses/by/4.0/ Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.
spellingShingle Review Article
Gossan, Nicole
Boot-Handford, Ray
Meng, Qing-Jun
Ageing and osteoarthritis: a circadian rhythm connection
title Ageing and osteoarthritis: a circadian rhythm connection
title_full Ageing and osteoarthritis: a circadian rhythm connection
title_fullStr Ageing and osteoarthritis: a circadian rhythm connection
title_full_unstemmed Ageing and osteoarthritis: a circadian rhythm connection
title_short Ageing and osteoarthritis: a circadian rhythm connection
title_sort ageing and osteoarthritis: a circadian rhythm connection
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4361727/
https://www.ncbi.nlm.nih.gov/pubmed/25078075
http://dx.doi.org/10.1007/s10522-014-9522-3
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