Conversely, in diabetic nephropathy and in HK-2 cells under hyperglycemic conditions, UCA1 is downregulated, and its overexpression attenuates apoptosis and inflammasome activation by targeting miR-206; luciferase/RIP assays confirm the UCA1–miR-206 interaction, and functional rescues demonstrate the axis anti-apoptotic effect in tubular epithelium [76]. Here, UCA1 is linked to diabetic kidney disease.