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Nrf2 in aging - Focus on the cardiovascular system.

Damian Kloska1, Aleksandra Kopacz1, Aleksandra Piechota-Polanczyk1

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Vascular Pharmacology
|September 1, 2018
PubMed
Summary

Aging accelerates cardiovascular diseases. Targeting the transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2) offers potential therapies, but its role in vascular aging and diseases is complex and cell-dependent.

Keywords:
AgingCardiovascular diseasesEndothelial cellsNrf2SenescenceVascular system

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Area of Science:

  • Cardiovascular Medicine
  • Cellular Aging
  • Molecular Biology

Background:

  • Aging is a primary risk factor for cardiovascular diseases (CVDs).
  • Cellular responses to aging are critical targets for CVD therapies.
  • The transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2) regulates cytoprotective and antioxidative genes.

Purpose of the Study:

  • To review the role of Nrf2 in cardiovascular diseases.
  • To discuss the impact of Nrf2 activity on vascular aging.
  • To explore the dualistic effects of Nrf2 in the context of vascular health and disease.

Main Methods:

  • Literature review of studies on Nrf2, aging, and cardiovascular diseases.
  • Analysis of Nrf2 expression and activity in various cell types within the cardiovascular system.
  • Synthesis of evidence regarding Nrf2's protective and detrimental roles.

Main Results:

  • Nrf2 expression correlates with lifespan in animal models.
  • Nrf2 activation can protect against oxidative stress and senescence in vascular cells.
  • Complete Nrf2 deficiency shows protective effects against atherosclerosis development, indicating context-dependent roles.

Conclusions:

  • Nrf2's role in cardiovascular diseases is complex and cell-type specific.
  • Targeting Nrf2 may offer therapeutic benefits for age-related cardiovascular conditions, but requires careful consideration of its dual functions.
  • Further research is needed to elucidate the precise mechanisms and therapeutic potential of Nrf2 modulation in vascular aging.