Non-coding RNAs in kidney injury and repair

Am J Physiol Cell Physiol. 2019 Aug 1;317(2):C177-C188. doi: 10.1152/ajpcell.00048.2019. Epub 2019 Apr 10.

Abstract

Acute kidney injury (AKI) is a major kidney disease featured by a rapid decline of renal function. Pathologically, AKI is characterized by tubular epithelial cell injury and death. Besides its acute consequence, AKI contributes critically to the development and progression of chronic kidney disease (CKD). After AKI, surviving tubular cells regenerate to repair. Normal repair restores tubular integrity, while maladaptive or incomplete repair results in renal fibrosis and eventually CKD. Non-coding RNAs (ncRNAs) are functional RNA molecules that are transcribed from DNA but not translated into proteins, which mainly include microRNAs (miRNAs), long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), small nucleolar RNAs (snoRNAs), and tRNAs. Accumulating evidence suggests that ncRNAs play important roles in kidney injury and repair. In this review, we summarize the recent advances in the understanding of the roles of ncRNAs, especially miRNAs and lncRNAs in kidney injury and repair, discuss the potential application of ncRNAs as biomarkers of AKI as well as therapeutic targets for treating AKI and impeding AKI-CKD transition, and highlight the future research directions of ncRNAs in kidney injury and repair.

Keywords: kidney injury; kidney repair; lncRNA; microRNA; non-coding RNA.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acute Kidney Injury / genetics
  • Acute Kidney Injury / metabolism*
  • Acute Kidney Injury / pathology
  • Acute Kidney Injury / physiopathology
  • Animals
  • Cell Proliferation
  • Disease Progression
  • Fibrosis
  • Gene Expression Regulation
  • Genetic Markers
  • Humans
  • Kidney / metabolism*
  • Kidney / pathology
  • Kidney / physiopathology
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • MicroRNAs / therapeutic use
  • RNA, Long Noncoding / genetics
  • RNA, Long Noncoding / metabolism*
  • RNA, Long Noncoding / therapeutic use
  • Regeneration*
  • Renal Insufficiency, Chronic / genetics
  • Renal Insufficiency, Chronic / metabolism*
  • Renal Insufficiency, Chronic / pathology
  • Renal Insufficiency, Chronic / physiopathology
  • Signal Transduction

Substances

  • Genetic Markers
  • MicroRNAs
  • RNA, Long Noncoding