端粒与骨关节炎软骨细胞衰老的研究进展

Research progress of telomere and chondrocyte senescence in osteoarthritis

骨关节炎是以软骨退变为特征的慢性退行性疾病,软骨细胞衰老在其发展中起着重要作用,但调控软骨细胞并决定衰老的具体机制尚未完全阐明。本文通过对端粒、端粒酶的结构和生物学效应,端粒在调节软骨细胞衰老过程中的关键机制,包括以慢性炎症、氧化应激、p53、pRb为标志的端粒缩短机制以及端粒酶活性降低所导致的端粒侵蚀,并对以SIRT6、MMP13、SA-β-Ga为主的软骨细胞衰老标志物的相关分子作用机制进行阐述,以期为骨关节炎的防治提供新的理论支撑。

Osteoarthritis is a chronic degenerative disease characterized by cartilage degenerations, and chondrocyte senescence is known to play an important role in the development of osteoarthritis, but its more specific mechanisms on regulating chondrocytes and determining their aging have not been fully clarified. This paper reviews the structure and their biological effects of telomere and telomerase, the key roles of telomeres in regulating the chondrocyte senescence, including the telomere shortening through the expressions of chronic inflammation, oxidative stress, p53, pRb and the telomere erosion caused by decreased telomerase activities,and summarizes the molecular mechanisms of SIRT6, MMP13 and SA-β-Ga as the main markers of chondrocyte senescence,hoping to provide a new theoretical support for the prevention and treatment of osteoarthritis.