Mitochondrial biogenesis: a potential therapeutic target for osteoarthritis

被引:34
作者
Blanco, F. J. [1 ,2 ]
Fernandez-Moreno, M. [2 ,3 ]
机构
[1] Complexo Hosp Univ A Coruna CHUAC, Agrupac Estrateg CICA INIBIC, Inst Invest Biomed A Coruna INIBIC, Grp Invest Reumatol, Sergas, Spain
[2] Univ A Coruna UDC, Dept Med, La Coruna, Spain
[3] Ctr Invest Biomed Red Bioingn Biomat & Nanomed CI, Madrid, Spain
关键词
Mitochondrial dynamics; Mfn2; Osteoarthritis; MITOFUSIN; 2; ENDOPLASMIC-RETICULUM; DYNAMICS; PARKIN; FISSION; FUSION; MFN2;
D O I
10.1016/j.joca.2020.03.018
中图分类号
R826.8 [整形外科学]; R782.2 [口腔颌面部整形外科学]; R726.2 [小儿整形外科学]; R62 [整形外科学(修复外科学)];
学科分类号
摘要
Mitochondrial dysfunction of human articular chondrocytes is considered a hallmark of cartilage degradation and OA pathogenesis. Due to the huge number of cellular processes in which mitochondria is implicated, even in the closed context of cellular respiration, the term mitochondrial function can refer to a variety of features which include fusion and fission, turnover (biogenesis and mitophagy), and plasticity. Mitochondrial biogenesis and mainly mitochondrial fusion and reduced mitophagy, contribute to the metabolic disorder and inflammation that occurs during OA. Reduced MFN2 and increased PARKIN expression represent potential therapeutic targets for the treatment of joint cartilage degradation during the OA process. (c) 2020 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:1003 / 1006
页数:4
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