AI Article Synopsis

  • Osteoarthritis (OA) is a common degenerative joint disease linked to mitochondrial dysfunction, which is crucial for energy production and cellular metabolism.
  • Mitochondrial dysfunction in OA is associated with increased oxidative stress, inflammation, abnormal chondrocyte metabolism, and impaired autophagy.
  • The review discusses potential interventions aimed at improving mitochondrial function to slow down or prevent the progression of OA, providing a deeper understanding of the disease's metabolic changes.

Article Abstract

Osteoarthritis (OA), a prevalent degenerative joint disease, affects a substantial global population. Despite the elusive etiology of OA, recent investigations have implicated mitochondrial dysfunction as a significant factor in disease pathogenesis. Mitochondria, pivotal cellular organelles accountable for energy production, exert essential roles in cellular metabolism. Hence, mitochondrial dysfunction can exert broad-ranging effects on various cellular processes implicated in OA development. This comprehensive review aims to provide an overview of the metabolic alterations occurring in OA and elucidate the diverse mechanisms through which mitochondrial dysfunction can contribute to OA pathogenesis. These mechanisms encompass heightened oxidative stress and inflammation, perturbed chondrocyte metabolism, and compromised autophagy. Furthermore, this review will explore potential interventions targeting mitochondrial metabolism as means to impede or decelerate the progression of OA. In summary, this review offers a comprehensive understanding of the involvement of mitochondrial metabolism in OA and underscores prospective intervention strategies.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11224101PMC
http://dx.doi.org/10.1007/s11010-023-04818-9DOI Listing

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