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During the resolution of inflammation, SPMs produced by polymorphonuclear cells and macrophages act to limit local tissue damage caused by inflammatory responses, including signaling cessation of polymorphonuclear cell infiltration, macrophage switching to an anti-inflammatory phenotype, apoptotic cell clearance, and reducing pain caused by nociceptor sensitization (49, 61)

Additionally, -Ketoglutarate(-KG) inhibited ferroptosis, significantly reducing matrix degradation and apoptosis in chondrocytes via the ETV4/SLC7A11/GPX4 signaling pathway, showing future clinical application prospects (He R