The role of NRF2 function and regulation in atherosclerosis: an update

Siarhei A Dabravolski1, Alexey V Churov2, Dmitry F Beloyartsev3

  • 1Department of Biotechnology Engineering, Braude Academic College of Engineering, Snunit 51, P.O. Box 78, 2161002, Karmiel, Israel. sergedobrowolski@gmail.com.

Insights

The nuclear factor erythroid 2-related factor 2 (NRF2) pathway and autophagy are key in atherosclerosis. Targeting these pathways and microRNAs may offer new treatments for cardiovascular disease.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Immunology

Background:

  • Atherosclerosis is a major cause of death globally, driven by chronic inflammation.
  • Understanding the molecular underpinnings of atherosclerosis is crucial for developing effective treatments.

Purpose of the Study:

  • To review the molecular mechanisms of the nuclear factor erythroid 2-related factor 2 (NRF2) pathway in atherosclerosis.
  • To explore the interplay between NRF2, autophagy, microRNAs (miRNAs), and atheroprotective genes.

Main Methods:

  • Literature review of molecular mechanisms in atherosclerosis.
  • Focus on the NRF2 pathway, autophagy, and miRNA regulation.
  • Identification of key genes and proteins involved in NRF2-mediated atheroprotection.

Main Results:

  • The NRF2/autophagy axis is critical for cellular responses to oxidative stress and inflammation in atherosclerosis.
  • Heat Shock Protein 90 (HSP90), Neuropeptide Y (NPY), and Glutaredoxin 2 (GLRX2) are key players.
  • MiRNAs significantly regulate gene expression impacting NRF2 signaling and disease susceptibility.
  • Genes like PDSS2, Srxn1, and IDH1 are involved in NRF2-dependent atheroprotective pathways.

Conclusions:

  • Targeting the NRF2/autophagy axis and miRNA networks holds therapeutic potential for atherosclerosis.
  • Further research is needed to elucidate complex interactions and develop novel interventions.
  • Modulating these pathways may improve cardiovascular outcomes by mitigating atherosclerosis progression.

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