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Mitochondrial biogenesis: a potential therapeutic target for osteoarthritis
F J Blanco1, M Fernández-Moreno2
1Grupo de Investigación en Reumatología, Instituto de Investigación Biomédica de A Coruña (INIBIC), Agrupación Estratégica CICA-INIBIC, Complexo Hospitalario Universitario de A Coruña (CHUAC), Sergas, Spain; Department of Medicine, Universidade de A Coruña (UDC), A Coruña, Spain.
Abstract:
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.
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