End-stage renal failure, reflux nephropathy and Feingold’s syndrome

Aslam, Mona; Bokhoven, Hans van; Taylor, Christopher M.

doi:10.1007/s00467-007-0602-3

Cited by 2 publications

(1 citation statement)

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“…In humans, miR-17~92 haploinsufficiency has been linked to Feingold Syndrome [28], a condition that is most frequently ascribed to mutations in n-Myc [36]. Renal defects have been reported in cases of Feingold Syndrome due to n-Myc mutations, including bilateral renal dysplasia and hypoplasia; however it remains unclear what role the miR-17~92 cluster plays during normal kidney development [36, 37]. Together, these data raise the question of whether a Pax2/n-Myc/ miR-17~92 pathway plays an important role in kidney development.…”

Section: A Potential Pax2/n-myc/mir-17~92 Interaction In Nephrogenesismentioning

confidence: 99%

MicroRNAs: potential regulators of renal development genes that contribute to CAKUT

Marrone

2013

Pediatr Nephrol

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Congenital anomalies of the kidney and urinary tract (CAKUT) are the leading cause of childhood chronic kidney disease (CKD). While mutations in several renal development genes have been identified as causes for CAKUT, most cases have not yet been linked to known mutations. Furthermore, the genotype-phenotype correlation is variable, suggesting that there are additional factors that impact the severity of CAKUT. MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression at the post-transcriptional level, and are involved in many developmental processes. Although little is known about the function of specific miRNAs in kidney development, several have recently been shown to regulate the expression of, and/or are regulated by, crucial renal development genes present in other organ systems. In this review, we discuss how miRNA regulation of common developmental signaling pathways may be applicable to renal development. We focus on genes that are known to contribute to CAKUT in humans, for which miRNA interactions in other contexts have been identified, with miRNAs that are present in the kidney. We hypothesize that miRNA-mediated processes play a role in kidney development through similar mechanisms, and speculate that genotypic variations in these small RNAs or their targets could be associated with CAKUT.

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