Despite intensive investigation of the role of microRNAs in AKI, a paucity of information exists regarding the role of microRNAs in kidney repair following AKI. A 2016 study used small RNA sequencing (RNA-seq) to generate temporal microRNA expression profiles, and 103 microRNAs were found to be differentially expressed during the injury and repair phase in a model of folic-acid-induced AKI171. Among these, three microRNAs were highly abundant and differentially expressed at different phases of injury: miR-18a-5p was induced during the acute injury phase, miR-132–3p was upregulated during the repair phase and miR-146b-5p was upregulated in the fibrotic phase. However, the function of these microRNAs was not investigated. Studies from the past few years have, however, indicated that some microRNAs that are induced during injury are possibly involved in kidney repair after AKI. For instance, induction of miR-687 during renal IRI inhibits PTEN to promote cell proliferation — an effect that might facilitate tissue repair or regeneration in ischaemic AKI175. On the other hand, miR-423–5p suppressed GSTM1 (glutathione-S-transferase Mu1) and inhibited cell proliferation, thereby preventing tissue repair following ischaemic AKI215. Similarly, miR-146b and miR-1247 limit kidney repair by inhibiting cell proliferation in cisplatin-induced or alcohol-induced AKI, respectively194,216.

Despite intensive investigation of the role of microRNAs in AKI, a paucity of information exists regarding the role of microRNAs in kidney repair following AKI. A 2016 study used small RNA sequencing (RNA-seq) to generate temporal microRNA expression profiles, and 103 microRNAs were found to be differentially expressed during the injury and repair phase in a model of folic-acid-induced AKI171. Among these, three microRNAs were highly abundant and differentially expressed at different phases of injury: miR-18a-5p was induced during the acute injury phase, miR-132–3p was upregulated during the repair phase and miR-146b-5p was upregulated in the fibrotic phase. However, the function of these microRNAs was not investigated. Studies from the past few years have, however, indicated that some microRNAs that are induced during injury are possibly involved in kidney repair after AKI. For instance, induction of miR-687 during renal IRI inhibits PTEN to promote cell proliferation — an effect that might facilitate tissue repair or regeneration in ischaemic AKI175. On the other hand, miR-423–5p suppressed GSTM1 (glutathione-S-transferase Mu1) and inhibited cell proliferation, thereby preventing tissue repair following ischaemic AKI215. Similarly, miR-146b and miR-1247 limit kidney repair by inhibiting cell proliferation in cisplatin-induced or alcohol-induced AKI, respectively194,216.