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Review
. 2020 Sep 7;21(18):6547.
doi: 10.3390/ijms21186547.

MicroRNAs in Chronic Kidney Disease: Four Candidates for Clinical Application

Linsey J F Peters  1   2   3   4 , Jürgen Floege  5 , Erik A L Biessen  1   2 , Joachim Jankowski  1   2 , Emiel P C van der Vorst  1   2   3   4   6
Affiliations
Review

MicroRNAs in Chronic Kidney Disease: Four Candidates for Clinical Application

Linsey J F Peters et al. Int J Mol Sci. .

Abstract

There are still major challenges regarding the early diagnosis and treatment of chronic kidney disease (CKD), which is in part due to the fact that its pathophysiology is very complex and not clarified in detail. The diagnosis of CKD commonly is made after kidney damage has occurred. This highlights the need for better mechanistic insight into CKD as well as improved clinical tools for both diagnosis and treatment. In the last decade, many studies have focused on microRNAs (miRs) as novel diagnostic tools or clinical targets. MiRs are small non-coding RNA molecules that are involved in post-transcriptional gene regulation and many have been studied in CKD. A wide array of pre-clinical and clinical studies have highlighted the potential role for miRs in the pathogenesis of hypertensive nephropathy, diabetic nephropathy, glomerulonephritis, kidney tubulointerstitial fibrosis, and some of the associated cardiovascular complications. In this review, we will provide an overview of the miRs studied in CKD, especially highlighting miR-103a-3p, miR-192-5p, the miR-29 family and miR-21-5p as these have the greatest potential to result in novel therapeutic and diagnostic strategies.

Keywords: MicroRNAs; chronic kidney disease; clinical application; kidney fibrosis.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
MicroRNA biosynthesis. First, the pri-miR is synthesized from the DNA by RNA polymerase II and is subsequently cleaved by Drosha and DGCR8 into pre-miR. The pre-miR is exported into the cytoplasm by Exportin-5 and Ran-GTP, followed by cleavage into a miR duplex by Dicer and TRBP. One strand is loaded into RISC consisting of AGO1, Dicer and TRBP. The RISC is guided to the target mRNA where the miR induces target degradation or translational repression of the mRNA. AGO1: argonaute 1; DGCR8: Drosha/DiGeorge syndrome critical region gene 8; pre-miR: primary microRNA; pre-mRNA: precursor messenger ribonucleic acid; Ran-GTP: GTP-binding nuclear protein Ran; RISC: RNA-induced silencing complex; RNA: ribonucleic acid; TRBP: tar RNA binding protein.
Figure 2
Figure 2
CKD-related microRNAs. All miRs that have until now been studied in CKD (ex-vivo or in-vivo models only) are depicted based on their relation to the specific pathologies. From all of these, the four relevant miRs that are highlighted in this review are visualized in bold. HN: hypertensive nephropathy, DKD: diabetic kidney disease, CVD: cardiovascular disease, CKD: chronic kidney disease.
See this image and copyright information in PMC

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