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.
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.