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衰老与骨关节炎中的细胞衰老

Cellular senescence in aging and osteoarthritis.

作者信息

Toh Wei Seong, Brittberg Mats, Farr Jack, Foldager Casper Bindzus, Gomoll Andreas H, Hui James Hoi Po, Richardson James B, Roberts Sally, Spector Myron

机构信息

a Faculty of Dentistry , National University of Singapore.

b Tissue Engineering Program , Life Sciences Institute, National University of Singapore , Singapore.

出版信息

Acta Orthop. 2016 Dec;87(sup363):6-14. doi: 10.1080/17453674.2016.1235087. Epub 2016 Sep 23.

DOI:10.1080/17453674.2016.1235087
PMID:27658487
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5389431/
Abstract
  • It is well accepted that age is an important contributing factor to poor cartilage repair following injury, and to the development of osteoarthritis. Cellular senescence, the loss of the ability of cells to divide, has been noted as the major factor contributing to age-related changes in cartilage homeostasis, function, and response to injury. The underlying mechanisms of cellular senescence, while not fully understood, have been associated with telomere erosion, DNA damage, oxidative stress, and inflammation. In this review, we discuss the causes and consequences of cellular senescence, and the associated biological challenges in cartilage repair. In addition, we present novel strategies for modulation of cellular senescence that may help to improve cartilage regeneration in an aging population.
摘要

人们普遍认为，年龄是损伤后软骨修复不良以及骨关节炎发展的一个重要促成因素。细胞衰老，即细胞分裂能力的丧失，已被视为导致软骨内环境稳定、功能及损伤反应发生与年龄相关变化的主要因素。细胞衰老的潜在机制虽尚未完全明确，但与端粒侵蚀、DNA损伤、氧化应激及炎症有关。在本综述中，我们讨论了细胞衰老的原因和后果，以及软骨修复中相关的生物学挑战。此外，我们还介绍了调节细胞衰老的新策略，这些策略可能有助于改善老年人群的软骨再生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f956/5389431/b6e8af535013/iort-87-6.F01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f956/5389431/b6e8af535013/iort-87-6.F01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f956/5389431/b6e8af535013/iort-87-6.F01.jpg

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WTAP mediates IL-1β-induced chondrocyte injury by enhancing CA12 mRNA stability depending on m6A modification.WTAP通过依赖m6A修饰增强CA12 mRNA稳定性来介导白细胞介素-1β诱导的软骨细胞损伤。
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