Stress response factors as hub-regulators of microRNA biogenesis: implication to the diseased heart

Veronika Gurianova1, Dmytro Stroy1, Rachele Ciccocioppo2

  • 1Bogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kiev, Ukraine.

Insights

MicroRNAs regulate heart function but contradictory data limits their therapeutic use. Understanding upstream regulators, like stress response factors, in the diseased heart can clarify their role and identify new cardiovascular disease therapies.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Epigenetics

Background:

  • MicroRNAs (miRNAs) are crucial regulators of cardiac function.
  • Existing data on miRNAs in cardiovascular disease present contradictions, hindering therapeutic development.
  • A deeper understanding of miRNA regulatory mechanisms is needed.

Purpose of the Study:

  • To elucidate hub-mechanisms governing microRNA biogenesis and function in the cardiovascular system.
  • To address and clarify contradictory findings in the field of miRNA research.
  • To identify potential therapeutic targets for cardiovascular diseases.

Main Methods:

  • Comprehensive review of literature on factors influencing miRNA biogenesis and function.
  • Analysis of stress response agents, epigenetic modifiers, splicing regulators, RNA editing, and protein homeostasis factors.
  • Examination of these factors' roles in cardiovascular function and miRNA regulation, particularly in cardiac pathologies.

Main Results:

  • Multiple factors, including stress response and epigenetic mediators, influence miRNA biogenesis and function.
  • The impact of these factors on miRNAs has been studied primarily in non-cardiac cells or specific cardiac conditions.
  • Identifying upstream regulators of miRNA biogenesis in diseased hearts is key.

Conclusions:

  • Studying stress response factors upstream of miRNA biogenesis in diseased hearts can resolve contradictions.
  • This approach will clarify the role of miRNAs in cardiovascular disease pathogenesis.
  • It will facilitate the development of novel molecular therapeutic targets for cardiovascular diseases.

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