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Chronic inflammation, metabolic stress, and certain lifestyle choices only further contribute to the decline

Pro-inflammatory adipokines (e.g., leptin, resistin) and adipose-derived exosomes (carrying miRNAs like miR-3074-5p) create a chronic inflammatory joint microenvironment by polarizing synovial macrophages toward an M1 phenotype and inhibiting anti-inflammatory adiponectin (1618)

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Nrf2 is involved in not only the regulation of GSH synthesis and reduction via upgrading some enzymes and proteins (SLC7A11, GCLM, GCLC, GR) but also the activation of GSH-dependent antioxidant enzymes (GPX, GST) [200, 201]

This confirmed that the injected GSH-high hES-MSCs induced a repair effect in the chondral defect sites rather than other endogenous factors, including surrounding host chondrocytes or endogenous MSCs

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