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细胞衰老与骨关节炎

Cellular aging towards osteoarthritis.

作者信息

Li Yu-Sheng, Xiao Wen-Feng, Luo Wei

机构信息

Department of Orthopaedics, Xiangya Hospital of Central South University, Changsha 410008, PR China.

Department of Orthopaedics, Xiangya Hospital of Central South University, Changsha 410008, PR China.

出版信息

Mech Ageing Dev. 2017 Mar;162:80-84. doi: 10.1016/j.mad.2016.12.012. Epub 2016 Dec 31.

Abstract

Osteoarthritis (OA) is a common form of degenerative joint disease. Aging process is supposed to be a leading predictor for developing OA. In this review, we have discussed the potential roles of aging in OA, a better understanding of which might delay or stop the development and progression of OA. Different cellular signaling mechanisms are involved process of aging that induces age-related changes in chondrocytes. These changes influence the expression of catabolic factors resulting in increased production of matrix metalloproteinases and cytokines, reduced levels of collagen type II and aggrecan synthesis, and increased production of reactive oxygen species (ROS). ROS leads to mitochondrial dysfunction and chondrocyte death, which contributes to the development of OA. Antioxidant supplementation is probably the best way to prevent or delay the age-related OA. Some therapeutic agents like histone deacetylase inhibitors and anti-miR34a agents have been reported to be effective against age-related OA. However, further research is needed to demonstrate the efficacy of these alternative treatment strategies in clinical trials using controlled and prospective studies.

摘要

骨关节炎(OA)是一种常见的退行性关节疾病。衰老过程被认为是发生骨关节炎的主要预测因素。在本综述中,我们讨论了衰老在骨关节炎中的潜在作用,更好地理解这一点可能会延缓或阻止骨关节炎的发展和进展。衰老过程涉及不同的细胞信号机制,这些机制会诱导软骨细胞发生与年龄相关的变化。这些变化影响分解代谢因子的表达,导致基质金属蛋白酶和细胞因子的产生增加、II型胶原蛋白和聚集蛋白聚糖合成水平降低,以及活性氧(ROS)的产生增加。ROS导致线粒体功能障碍和软骨细胞死亡,这有助于骨关节炎的发展。补充抗氧化剂可能是预防或延缓与年龄相关的骨关节炎的最佳方法。据报道,一些治疗药物如组蛋白去乙酰化酶抑制剂和抗miR34a药物对与年龄相关的骨关节炎有效。然而,需要进一步的研究来在使用对照和前瞻性研究的临床试验中证明这些替代治疗策略的疗效。

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