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Role of redoximiRs in fibrogenesis

Marta Fierro-Fernández1, Verónica Miguel1, Santiago Lamas1

  • 1Department of Cell Biology and Immunology, Centro de Biología Molecular "Severo Ochoa" (CBMSO), Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, Nicolás Cabrera 1, 28049 Madrid, Spain.

Redox Biology
|December 15, 2015
PubMed

Insights

Fibrosis involves excessive extracellular matrix buildup. New research explores how microRNAs (miRNAs) regulating oxidative stress, termed "redoxifibromiRs," impact fibrotic processes.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Genetics

Background:

  • Fibrosis is characterized by excessive extracellular matrix accumulation, leading to tissue scarring and dysfunction.
  • MicroRNAs (miRNAs) are key regulators of gene expression, influencing various biological processes.
  • Oxidative stress is a critical factor in the progression of fibrotic diseases.

Purpose of the Study:

  • To review the mechanisms through which specific microRNAs, termed "redoxifibromiRs," regulate fibrogenesis.
  • To highlight the role of miRNAs in controlling oxidative stress pathways relevant to fibrosis.
  • To introduce the concept of "redoxifibromiRs" as a novel class of fibromiRs.

Main Methods:

  • Literature review of studies on microRNAs, fibrosis, and oxidative stress.
  • Analysis of miRNA-mediated regulation of genes involved in reactive oxygen species (ROS) production and antioxidant defense.
  • Synthesis of current knowledge on the interplay between redox signaling and fibrotic pathways.

Main Results:

  • MicroRNAs (miRNAs) act as potent regulators of fibrotic processes, known as "fibromiRs."
  • Specific miRNAs, termed "redoximiRs," modulate the expression of genes related to oxidative stress.
  • These "redoximiRs" are implicated in the self-perpetuating mechanisms of fibrogenesis.

Conclusions:

  • "RedoxifibromiRs" represent a newly identified class of microRNAs that bridge redox regulation and fibrosis.
  • Understanding "redoxifibromiRs" offers potential therapeutic targets for treating fibrotic diseases.
  • Targeting these "redoxifibromiRs" could disrupt the link between oxidative stress and excessive matrix deposition in fibrosis.
Keywords:
FibrosisMicroRNAsOxidative stress

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