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Nrf2 Deficiency Unmasks the Significance of Nitric Oxide Synthase Activity for Cardioprotection

Ralf Erkens1, Tatsiana Suvorava1, Thomas R Sutton2,3

  • 1Cardiovascular Research Laboratory, Division of Cardiology, Pulmonology and Vascular Medicine, Medical Faculty, Heinrich Heine University, Moorenstrasse 5, 40225 Düsseldorf, Germany.

Oxidative Medicine and Cellular Longevity
|June 2, 2018
PubMed

Insights

Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) deficiency surprisingly reduced heart attack size after ischemia/reperfusion injury. This suggests endothelial nitric oxide synthase (eNOS) upregulation may protect the heart when antioxidant capacity is low.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Oxidative Stress Research

Background:

  • Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is a transcription factor regulating antioxidant and cytoprotective enzymes.
  • Nrf2 plays a critical role in cellular defense against oxidative stress and injury.

Purpose of the Study:

  • To investigate the impact of Nrf2 deficiency on myocardial ischemia/reperfusion (I/R) injury.
  • To determine the role of Nrf2 in regulating antioxidative capacity, redox state, and nitric oxide (NO) metabolism during I/R.

Main Methods:

  • Utilized Nrf2 knockout (Nrf2 KO) and wild-type (WT) mice to study myocardial I/R injury.
  • Measured infarct size, left ventricular function, eNOS expression, and NO metabolite concentrations.
  • Investigated the effects of nitric oxide synthase (NOS) inhibition in Nrf2 KO and WT mice.

Main Results:

  • Nrf2 KO mice exhibited smaller infarct size and preserved cardiac function post-I/R compared to WT mice.
  • Nrf2 deficiency led to elevated eNOS expression and maintained NO metabolite levels.
  • Inhibition of NO synthesis exacerbated myocardial damage in Nrf2 KO mice, but not in WT mice.

Conclusions:

  • Upregulation of eNOS may confer cardioprotection against I/R injury, particularly under conditions of diminished antioxidant capacity.
  • Nrf2-dependent antioxidant pathways can mask the protective role of eNOS under normal conditions.
  • These findings highlight a potential therapeutic strategy targeting eNOS for I/R injury management.

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