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The synovial fluid of HUA patients culled from joint tissues demonstrates an expression of RANTES and MCP-1, insinuating that UA may indirectly enhance the inflammatory response within the joint by elevating chemokine expression and enlisting monocytes
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Experimental verification showed that the inhibition of the mitochondrial ROS-mediated pathway enhances insulin production from pancreatic cells [88], subsequently causing ferroptosis due to the accumulation of lipid peroxides [89]