Abstract
IgA nephropathy is globally the most common primary glomerulonephritis, but the pathogenesis of this condition is still only partially understood. MicroRNAs (miRNAs) are short, noncoding RNA molecules that regulate gene expression. Genome-wide analysis of renal miRNA expression has identified a number of novel miRNAs related to immunological and pathological changes. Specifically, overexpression of miR-148b might explain the aberrant glycosylation of IgA1, which has a central pathogenetic role in the early phase of IgA nephropathy. By contrast, miR-29c is an antifibrotic miRNA that is probably important in the late stages of disease progression. In addition, urinary levels of several miRNAs are significantly changed in patients with IgA nephropathy compared with healthy individuals; some alterations seem to be disease-specific, whereas others are apparently damage-related. As miRNAs in urinary sediment are relatively stable and easily quantified, they have the potential to be used as biomarkers for the diagnosis and monitoring of disease. However, to date, limited data are available on the role of miRNAs in the pathogenesis of IgA nephropathy and their potential application as biomarkers. Consequently, further studies are urgently needed to address this shortfall. Here, we review the available literature on miRNAs in relation to IgA nephropathy.
Highlights
IgA nephropathy (IgAN) is the most common primary glomerulonephritis in the world
That study described the relationship of the urinary sediment miR200 family, miR-205, and miR-192 in IgAN with the severity of IgAN renal injury and IgAN prognosis; it even speculated the mechanisms by which these three miRNAs affect renal fibrosis and provided new ideas for the study of miRNAs in IgAN
148b was a key in the pathogenesis of IgAN, which could result in galactose deficient IgA1 in IgAN
Summary
IgA nephropathy (IgAN) is the most common primary glomerulonephritis in the world. Approximately 20–40% of patients with IgAN develop the end-stage renal disease (ESRD) within 10–20 years [1,2]; IgAN is one of the main causes of ESRD [3,4,5,6,7]. That study described the relationship of the urinary sediment miR200 family, miR-205, and miR-192 in IgAN with the severity of IgAN renal injury and IgAN prognosis; it even speculated the mechanisms by which these three miRNAs affect renal fibrosis and provided new ideas for the study of miRNAs in IgAN. Studies of miRNAs have mainly focused on the mechanisms by which miRNAs influence the pathogenesis of IgAN, the association between miRNAs and the severity of IgAN, and the relationship between miRNAs and the prognosis of IgAN. The potential value of miRNAs as biomarkers in IgAN has gradually developed, especially for miRNAs in urine sediment. We provide a detailed review of the effects of miRNAs on the pathogenesis and development of IgAN, their relationship with the severity of renal damage in IgAN, as well as their potential in diagnosis and predicting prognosis of IgAN
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