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. 2026 Feb 25;17:1671502. doi: 10.3389/fimmu.2026.1671502

Figure 1.

Infographic illustrating osteoarthritis and its core feature, cartilage degeneration, linked to high incidence, disability, burden, limited treatment, prosthetic longevity, and efficacy. Cartilage degeneration results from abnormal behavior and fate, driven by disordered mitochondrial quality control, including impairment in redox, biogenesis, dynamics, and mitophagy. Contributing cell behaviors are synthesis/catabolism imbalance, cluster formation, autophagy dysregulation, hypertrophy, and senescence. Aberrant fate outcomes include abnormal chondrogenesis, apoptosis, necrosis, chondroptosis, necroptosis, autophagic cell death, pyroptosis, and ferroptosis, emphasizing mitochondrial dysfunction’s role in osteoarthritis pathology and management challenges.

OA is highly prevalent, disabling and burdensome, with limited current treatments and prosthetic longevity. Centered on cartilage degeneration, disordered MQC accelerates this process by regulating chondrocyte aberrant behaviors and diverse cell death modalities.