Therapeutic potential of microRNAs for the treatment of renal fibrosis and CKD

Abstract

Chronic kidney disease (CKD), defined as reduced glomerular filtration rate, is increasingly becoming a major public health issue. At the histological level, renal fibrosis is the final common pathway leading to end-stage renal disease, irrespective of the initial injury. According to this view, antifibrotic agents should slow or halt the progression of CKD. However, due to multiple overlapping pathways stimulating fibrosis, it has been difficult to develop antifibrotic drugs that delay or reverse the progression of CKD. MicroRNAs (miRNAs) are small noncoding RNA molecules, 18-22 nucleotides in length, that control many developmental and cellular processes as posttranscriptional regulators of gene expression. Emerging evidence suggests that miRNAs targeted against genes involved in renal fibrosis might be potential candidates for the development of antifibrotic therapies for CKD. This review will discuss some of the miRNAs, such as Let-7, miR-21,-29, -192, -200,-324, -132, -212, -30, -126, -433, -214, and -199a, that are implicated in renal fibrosis and the potential to exploit these molecular targets for the treatment of CKD.

Urine biomarkers of chronic kidney damage and renal functional decline in childhood-onset systemic lupus erythematosus

“…Unfortunately, our findings are in line with those of many other investigators that aimed at validating urine biomarkers of kidney damage [46]. Arguably, blood-based biomarkers [47], microRNAs reflecting renal fibrosis [48], and/or advanced kidney imaging strategies [49] might be better suited to capture abnormalities in renal mechanisms due to structural changes with LN chronicity.…”

Genetic deficiency or pharmacological inhibition of miR-33 protects from kidney fibrosis

“…miRNAs have emerged as powerful regulators of fibrotic processes in the kidney (55,56). Thus, Gomez et al identified 24 miRNAs that were commonly upregulated both in human CKD and in animal models of kidney injury, suggesting a "fibrotic" miRNA signature in the kidney (18).…”

<p>Silibinin Augments the Antifibrotic Effect of Valsartan Through Inactivation of TGF-β1 Signaling in Kidney</p>

“…1 When renal fibrosis occurs, most of the patients will develop to chronic kidney disease (CKD), following with end-stage renal disease (ESRD). 4 In that situation, transplantation is the only effective therapeutic strategy. 5 In addition, it has been reported that patients with CKD account for 10% of the world's population.…”

“…5 In addition, it has been reported that patients with CKD account for 10% of the world's population. 4 Therefore, novel effective strategy that inhibits progression of renal fibrosis caused by diabetic nephropathy is of great importance.…”