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Potential Targeting of Renal Fibrosis in Diabetic Kidney Disease Using MicroRNAs. | LitMetric

AI Article Synopsis

  • - Diabetic kidney disease (DKD) is a significant global health issue, leading to end-stage renal disease and characterized by excessive protein buildup in kidney structures, resulting in fibrosis.
  • - Current research highlights the potential of targeting specific pathways, such as the activation of the Nrf2 pathway and inhibition of TGF-beta signaling, for developing effective DKD therapies.
  • - MicroRNAs (miRNAs) are small RNA molecules that play a role in regulating gene expression and have been implicated in renal fibrosis; there is growing interest in using them as a treatment strategy for DKD.

Article Abstract

Diabetic kidney disease (DKD) is a major health problem and one of the leading causes of end-stage renal disease worldwide. Despite recent advances, there exists an urgent need for the development of new treatments for DKD. DKD is characterized by the excessive synthesis and deposition of extracellular matrix proteins in glomeruli and the tubulointerstitium, ultimately leading to glomerulosclerosis as well as interstitial fibrosis. Renal fibrosis is the final common pathway at the histological level leading to an end-stage renal failure. In fact, activation of the nuclear factor erythroid 2-related factor 2 pathway by bardoxolone methyl and inhibition of transforming growth factor beta signaling by pirfenidone have been assumed to be effective therapeutic targets for DKD, and various basic and clinical studies are currently ongoing. MicroRNAs (miRNAs) are endogenously produced small RNA molecules of 18-22 nucleotides in length, which act as posttranscriptional repressors of gene expression. Studies have demonstrated that several miRNAs contribute to renal fibrosis. In this review, we outline the potential of using miRNAs as an antifibrosis treatment strategy and discuss their clinical application in DKD.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7751689PMC
http://dx.doi.org/10.3389/fphar.2020.587689DOI Listing

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