骨关节炎的细胞老化机制。

P K Sacitharan, T L Vincent
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引用次数: 28

摘要

年龄是骨关节炎(OA)发展的最大独立风险因素,多年来,这被认为是由于关节表面随时间的重复性微创伤,即所谓的“磨损性”关节炎。随着我们对OA发病机制的理解越来越完善,它改变了我们对衰老在疾病中的作用的认识。软骨在疾病中的破坏不是一个被动的过程,而是一个涉及特定基质降解酶的诱导和激活的过程;软骨细胞对关节的机械、炎症和代谢环境的变化非常敏感;软骨通过改变其基质不断适应这些变化。衰老会影响所有这些过程。在这篇综述中,我们将讨论衰老如何影响组织结构,关节使用和细胞代谢。我们描述了其他模型系统中与衰老相关的已知途径,并讨论了针对OA中这些途径的潜在价值。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Cellular ageing mechanisms in osteoarthritis.

Cellular ageing mechanisms in osteoarthritis.

Cellular ageing mechanisms in osteoarthritis.

Cellular ageing mechanisms in osteoarthritis.

Age is the strongest independent risk factor for the development of osteoarthritis (OA) and for many years this was assumed to be due to repetitive microtrauma of the joint surface over time, the so-called 'wear and tear' arthritis. As our understanding of OA pathogenesis has become more refined, it has changed our appreciation of the role of ageing on disease. Cartilage breakdown in disease is not a passive process but one involving induction and activation of specific matrix-degrading enzymes; chondrocytes are exquisitely sensitive to changes in the mechanical, inflammatory and metabolic environment of the joint; cartilage is continuously adapting to these changes by altering its matrix. Ageing influences all of these processes. In this review, we will discuss how ageing affects tissue structure, joint use and the cellular metabolism. We describe what is known about pathways implicated in ageing in other model systems and discuss the potential value of targeting these pathways in OA.

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