Fig. 8: Schematic illustration of the regulatory role of the USP32-PKM2 axis in temporomandibular joint osteoarthritis (TMJOA) pathogenesis. | Cell Death & Disease

Fig. 8: Schematic illustration of the regulatory role of the USP32-PKM2 axis in temporomandibular joint osteoarthritis (TMJOA) pathogenesis.

From: USP32 promotes temporomandibular joint osteoarthritis by modulating PKM2 stability and glycolytic metabolism in chondrocytes

Fig. 8

This diagram illustrates the regulatory role of the ubiquitin-specific protease 32 (USP32)-pyruvate kinase M2 (PKM2) axis in TMJOA progression. Under pathological conditions, USP32 is upregulated in TMJOA cartilage and inflammatory chondrocytes, where it stabilizes PKM2 by removing K48- and K11-linked ubiquitin chains, preventing its proteasomal degradation. Excessive accumulation of PKM2 promotes glycolysis and lactate accumulation while impairing mitochondrial function. The metabolic shift exacerbates chondrocyte apoptosis and extracellular matrix (ECM) degradation, contributing to TMJOA pathology.

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