title: Autophagy in osteoarthritis.
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.
authors.affiliation: Department of Orthopaedics, Xiangya Hospital, Central South University, No. 87 Xiangya Road, Changsha, Hunan 410008, PR China.
authors.forename: Yu-Sheng
authors.initials: YS
authors.lastname: Li
authors.affiliation: Department of Emergency Medicine, Xiangya Hospital, Central South University, No. 87 Xiangya Road, Changsha, Hunan 410008, PR China.
authors.forename: Fang-Jie
authors.initials: FJ
authors.lastname: Zhang
authors.affiliation: Department of Orthopaedics, Xiangya Hospital, Central South University, No. 87 Xiangya Road, Changsha, Hunan 410008, PR China.
authors.forename: Chao
authors.initials: C
authors.lastname: Zeng
authors.affiliation: Department of Orthopaedics, Xiangya Hospital, Central South University, No. 87 Xiangya Road, Changsha, Hunan 410008, PR China.
authors.forename: Wei
authors.initials: W
authors.lastname: Luo
authors.affiliation: Department of Orthopaedics, Xiangya Hospital, Central South University, No. 87 Xiangya Road, Changsha, Hunan 410008, PR China.
authors.forename: Wen-Feng
authors.initials: WF
authors.lastname: Xiao
authors.affiliation: Department of Orthopaedics, Xiangya Hospital, Central South University, No. 87 Xiangya Road, Changsha, Hunan 410008, PR China.
authors.forename: Shu-Guang
authors.initials: SG
authors.lastname: Gao
authors.affiliation: Department of Orthopaedics, Xiangya Hospital, Central South University, No. 87 Xiangya Road, Changsha, Hunan 410008, PR China. Electronic address: lghxycsu@126.com.
authors.forename: Guang-Hua
authors.initials: GH
authors.lastname: Lei
mesh_terms: D001343:Autophagy / Q000187:drug effects / Q000502:physiology*; D002358:Cartilage, Articular / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology*; D019902:Chondrocytes / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D007166:Immunosuppressive Agents / Q000494:pharmacology / Q000627:therapeutic use; D007249:Inflammation / Q000503:physiopathology; D010003:Osteoarthritis / Q000188:drug therapy / Q000503:physiopathology*; D020123:Sirolimus / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D007166:Immunosuppressive Agents; D020123:Sirolimus
keywords: Autophagy; Chondrocyte; Osteoarthritis; Rapamycin