We mainly focus on revealing the functions of miRNAs (e.g., miR-21, miR-24, miR-30 family, miR-126, miR-127, miR-150, miR-494 and miR-687) and lncRNAs (e.g., TapSAKI, AK139328 and lncRNA-PRINS) in the pathogenesis of AKI.
MiR-210 and miR-494 expression was significantly decreased and miR-205 expression was increased in survivors with sepsis-induced AKI (28-day survival, n = 68) vs. non-survivors (n = 42).
Gain-and-loss-of-function studies demonstrated that miRNAs, such as miR-24, miR-126, miR-494, and miR-687, may bind to the 3'-untranslated region of their target genes to regulate inflammation, programmed cell death, and cell cycle in the injury and repair stages of AKI, indicating their therapeutic potential in AKI.