MicroRNA function in the profibrogenic interplay upon chronic liver disease

Int J Mol Sci. 2014 May 27;15(6):9360-71. doi: 10.3390/ijms15069360.

Abstract

In chronic liver disease leading to fibrosis, hepatic stellate cells (HSC) differentiate into myofibroblasts. Myofibroblastic HSC have taken center stage during liver fibrogenesis, due to their remarkable synthesis of extracellular matrix proteins, their secretion of profibrogenic mediators and their contribution to hypertension, due to elevated contractility. MicroRNAs (miRNAs) are small, noncoding RNA molecules of 19-24 nucleotides in length. By either RNA interference or inhibition of translational initiation and elongation, each miRNA is able to inhibit the gene expression of a wide panel of targeted transcripts. Recently, it was shown that altered miRNA patterns after chronic liver disease highly affect the progression of fibrosis by their potential to target the expression of extracellular matrix proteins and the synthesis of mediators of profibrogenic pathways. Here, we underline the role of miRNAs in the interplay of the profibrogenic cell communication pathways upon myofibroblastic differentiation of hepatic stellate cells in the chronically injured liver.

Publication types

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

MeSH terms

  • Animals
  • Chronic Disease
  • Gene Expression Regulation
  • Hepatic Stellate Cells / metabolism
  • Hepatic Stellate Cells / pathology*
  • Humans
  • Liver / metabolism
  • Liver / pathology*
  • Liver Cirrhosis / etiology*
  • Liver Cirrhosis / genetics
  • Liver Cirrhosis / metabolism
  • Liver Cirrhosis / pathology
  • Liver Diseases / complications*
  • Liver Diseases / genetics*
  • Liver Diseases / metabolism
  • Liver Diseases / pathology
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • Myofibroblasts / metabolism
  • Myofibroblasts / pathology*
  • Signal Transduction

Substances

  • MicroRNAs