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Joint Bone Spine
Volume 83, n° 2
pages 143-148 (mars 2016)
Doi : 10.1016/j.jbspin.2015.06.009
accepted : 21 June 2015
Autophagy in osteoarthritis
 

Yu-Sheng Li a, Fang-Jie Zhang b, Chao Zeng a, Wei Luo a, Wen-Feng Xiao a, Shu-Guang Gao a, Guang-Hua Lei a,
a Department of Orthopaedics, Xiangya Hospital, Central South University, No. 87 Xiangya Road, Changsha, Hunan 410008, PR China 
b Department of Emergency Medicine, Xiangya Hospital, Central South University, No. 87 Xiangya Road, Changsha, Hunan 410008, PR China 

Corresponding author.
Abstract

Degradation of the articular cartilage is at the centre of the pathogenesis of osteoarthritis (OA), for which age is the major risk factor. Maintaining the chondrocytes in a healthy condition appears to be an important factor for preservation of the entire cartilage and preventing its degeneration. Autophagy, which is an essential cellular homeostatic mechanism for the removal of dysfunctional cellular organelles and macromolecules, is increased by catabolic and nutritional stresses. Autophagy is increased in OA chondrocytes and cartilage, particularly during the initial degenerative phase, to regulate changes in OA-like gene expression through modulation of apoptosis and reactive oxygen species (ROS). In this way, autophagy acts as an adaptive response to protect chondrocytes from various environmental changes, while with gradual cartilage degradation, decreased autophagy is linked with cell death. Rapamycin, which is a specific inhibitor of the mTOR signaling pathway, enhances expression of autophagy regulators and prevents chondrocyte death. In the future, pharmacological activation of autophagy may be an effective therapeutic approach for OA.

The full text of this article is available in PDF format.

Keywords : Autophagy, Chondrocyte, Osteoarthritis, Rapamycin




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