MicroRNAs in diabetic nephropathy: From molecular mechanisms to new therapeutic targets of treatment

Biochem Pharmacol. 2021 Jul:189:114301. doi: 10.1016/j.bcp.2020.114301. Epub 2020 Oct 23.

Abstract

Despite considerable investigation in diabetic nephropathy (DN) pathogenesis and possible treatments, current therapies still do not provide competent prevention from disease progression to end-stage renal disease (ESRD) in most patients. Therefore, investigating exact molecular mechanisms and important mediators underlying DN may help design better therapeutic approaches for proper treatment. MicroRNAs (MiRNAs) are a class of small non-coding RNAs that play a crucial role in post-transcriptional regulation of many gene expression within the cells and present an excellent opportunity for new therapeutic approaches because their profile is often changed during many diseases, including DN. This review discusses the most important signaling pathways involved in DN and changes in miRNAs profile in each signaling pathway. We also suggest possible approaches for miRNA derived interventions for designing better treatment of DN.

Keywords: Diabetic nephropathy; End-stage renal disease; MicroRNAs; TGF-β signaling pathway; Therapeutic targets.

Publication types

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

MeSH terms

  • Animals
  • Diabetes Mellitus / drug therapy
  • Diabetes Mellitus / genetics
  • Diabetes Mellitus / metabolism
  • Diabetic Nephropathies / genetics
  • Diabetic Nephropathies / metabolism*
  • Diabetic Nephropathies / therapy*
  • Gene Targeting / methods
  • Gene Targeting / trends*
  • Humans
  • MicroRNAs / administration & dosage*
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Signal Transduction / drug effects
  • Signal Transduction / physiology
  • Transforming Growth Factor beta / antagonists & inhibitors
  • Transforming Growth Factor beta / genetics
  • Transforming Growth Factor beta / metabolism
  • Treatment Outcome

Substances

  • MicroRNAs
  • Transforming Growth Factor beta