MicroRNAs, a class of small non-coding RNAs that act as post-transcriptional regulators of gene expression, have attracted increasing attention as critical regulators of organogenesis, cancer and disease. Interest has been spurred by development of a novel class of synthetic RNA oligonucleotides with excellent drug-like properties that hybridize to a specific microRNA preventing its action. In kidney disease, a small number of microRNAs, are dysregulated. These overlap with regulated microRNA in nephrogenesis and kidney cancers. Several dysregulated microRNA have been identified in fibrotic diseases of other organs, representing a 'fibrotic signature', and some of these fibrotic microRNA contribute remarkably to the pathogenesis of kidney disease. Chronic kidney disease affecting ∼10% of the population, leads to kidney failure, with few treatment options. Here we will explore the pathological mechanism of miR-21, whose pre-eminent role in amplifying kidney disease and fibrosis by suppressing mitochondrial biogenesis and function is established. Evolving roles for miR-214, -199, -200, -155, -29, -223 and -126 in kidney disease will be discussed, and we will demonstrate how studying function of distinct microRNAs has led to new mechanistic insights for kidney disease progression. Finally, the utility of anti-miRNA oligonucleotides as potential novel therapeutics to treat chronic disease will be highlighted.
- Copyright © 2015, American Journal of Physiology - Renal Physiology