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Physiological and pathological functions of NADPH oxidases during myocardial ischemia-reperfusion

Shouji Matsushima1, Hiroyuki Tsutsui2, Junichi Sadoshima3

  • 1Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, Rutgers-New Jersey Medical School, Newark, NJ; Department of Cardiovascular Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan.

Trends in Cardiovascular Medicine
|June 2, 2014
PubMed

Insights

Oxidative stress in the heart involves reactive oxygen species (ROS). NADPH oxidase (Nox) 2 and 4 play dual roles in heart injury, with balanced ROS essential for protection during ischemia-reperfusion.

Area of Science:

  • Cardiovascular Biology
  • Oxidative Stress Research
  • Molecular Cardiology

Background:

  • Oxidative stress, an imbalance between reactive oxygen species (ROS) and antioxidants, causes myocardial damage, contributing to ischemic heart disease and heart failure.
  • NADPH oxidase (Nox) isoforms, particularly Nox2 and Nox4, are key sources of cardiac ROS and regulate cardiomyocyte survival and growth.
  • Both Nox2 and Nox4 are upregulated during ischemia-reperfusion (I/R), exacerbating myocardial injury through increased ROS production.

Purpose of the Study:

  • To investigate the dual role of Nox2 and Nox4 in regulating myocardial injury during ischemia-reperfusion (I/R).
  • To elucidate the complex relationship between ROS levels, Nox isoform activity, and cardiomyocyte response to I/R.
  • To discuss the detrimental and beneficial functions of Nox isoforms in the context of myocardial I/R.

Main Methods:

  • Review and discussion of existing literature on Nox isoforms, ROS production, and myocardial I/R injury.
  • Analysis of the roles of Nox2 and Nox4 in regulating cardiomyocyte growth, death, and response to oxidative stress.
  • Examination of the impact of Nox suppression on I/R injury and the involvement of signaling pathways like HIF-1α and PPARα.

Main Results:

  • While suppression of either Nox2 or Nox4 can reduce ROS and I/R injury, a basal level of ROS produced by these isoforms is crucial for cardioprotection.
  • A minimum ROS level generated by Nox2 or Nox4 is necessary for activating HIF-1α and inhibiting PPARα during I/R.
  • Combined suppression of both Nox2 and Nox4 worsens myocardial I/R injury, indicating that complete abolition of ROS is detrimental.

Conclusions:

  • Both excessive ROS production and insufficient ROS signaling via Nox isoforms can lead to cardiac injury during I/R.
  • Maintaining a physiological level of ROS, regulated by Nox2 and Nox4, is essential for myocardial protection against I/R.
  • Targeting Nox isoforms requires a nuanced approach, considering their dual roles to avoid exacerbating cardiac damage.

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