Abstract
Osteoarthritis (OA) is a common and disabling joint disorder that is mainly characterized by cartilage degeneration and narrow joint spaces. The role of mitochondrial dysfunction in promoting the development of OA has gained much attention. Targeting endogenous molecules to improve mitochondrial function is a potential treatment for OA. Moreover, research on exogenous drugs to improve mitochondrial function in OA based on endogenous molecular targets has been accomplished. In addition, stem cells and exosomes have been deeply researched in the context of cartilage regeneration, and these factors both reverse mitochondrial dysfunctions. Thus, we hypothesize that biomedical approaches will be applied to the treatment of OA. Furthermore, we have summarized the global status of mitochondria and osteoarthritis research in the past two decades, which will contribute to the research field and the development of novel treatment strategies for OA.
Highlights
Osteoarthritis (OA), a chronic and progressive cartilage degeneration disease [1] with a high morbidity and disability rate [2], is characterized by cartilage degeneration, osteophyte formation, thickening of subchondral bone, synovial inflammation, and meniscal injuries [3]
Studies have shown that mitochondrial dysfunction with reduced membrane potential (MMP) and increased mitochondrial membrane permeability could promote the migration of cytochrome C (Cyt-C) from the mitochondrial matrix to the cytoplasm [87], which could induce apoptosis due to the activation of caspases and increase the BCL2-associated X protein (BAX)/Bcl-2 ratio [88]
We found that “Phenotype,” “SIRT3,” “PCG-1α,” “AMPK,” “FOXO transcription factors,” “Mitophagy,” “Acetylation,” “Nuclear transcription factor erythroid-2-like factor 2 (Nrf2),” and “Repair,” which were red colored, occurred recently, which may mean that research on mitochondria and osteoarthritis will focus on mechanistic studies and cartilage repair
Summary
Osteoarthritis (OA), a chronic and progressive cartilage degeneration disease [1] with a high morbidity and disability rate [2], is characterized by cartilage degeneration, osteophyte formation, thickening of subchondral bone, synovial inflammation, and meniscal injuries [3]. Chondrocyte apoptosis induced by inflammation, oxidative stress, and increased mitochondrial membrane permeability [81] is positively associated with the degree of cartilage damage [82, 83]. Studies have shown that mitochondrial dysfunction with reduced MMP and increased mitochondrial membrane permeability could promote the migration of Cyt-C from the mitochondrial matrix to the cytoplasm [87], which could induce apoptosis due to the activation of caspases and increase the BAX/Bcl-2 ratio [88]. The accumulation of mtDNA mutations above a critical level could lead to dysfunction of the respiratory chain and increased ROS production, which could promote excessive chondrocyte apoptosis and enhance inflammatory responses [8]. Melatonin and its metabolites can remove ROS by radical scavenging and improve the activation of antioxidant enzymes,
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