The role and intervention of mitochondrial metabolism in osteoarthritis

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.

Editorial: New trends in osteoarthritis treatment

“…Mitochondrial function could represent a target for OA treatment ( 17 ). Mao et al reviewed mitochondrial dysfunctions in OA chondrocytes reported as decreased ATP production, increased oxidative stress, calcium dysregulation, increased permeability of the mitochondrial membrane, mtDNA alternations, and activation of mitochondrial apoptotic pathway resulting in cartilage degeneration.…”