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Nitrite-Nitric Oxide Signaling and Cardioprotection

Matthias Totzeck1, Ulrike B Hendgen-Cotta1, Tienush Rassaf2

  • 1Department of Cardiology and Vascular Medicine, West German Heart and Vascular Center, University Hospital Essen, Essen, Germany.

Advances in Experimental Medicine and Biology
|May 29, 2017
PubMed

Insights

Nitric oxide (NO) signaling protects the heart from ischemia/reperfusion injury by reducing reactive oxygen species (ROS) and improving mitochondrial function. Therapeutic strategies targeting NO pathways offer promising cardioprotection for myocardial infarction patients.

Area of Science:

  • Cardiovascular Research
  • Mitochondrial Biology
  • Cellular Signaling

Background:

  • Acute myocardial infarction causes lethal ischemia/reperfusion (I/R) injury, partly due to mitochondrial damage.
  • Mitochondrial damage in I/R involves reactive oxygen species (ROS), calcium dysregulation, outer membrane permeabilization, and altered dynamics.
  • Nitric oxide (NO) signaling is a recognized cardioprotective mechanism against I/R injury.

Purpose of the Study:

  • To elucidate the role of NO signaling in cardiomyocyte protection during myocardial I/R injury.
  • To explore the mechanisms of NO-mediated cardioprotection, focusing on mitochondrial posttranslational modifications.
  • To discuss therapeutic strategies for leveraging NO signaling in clinical cardioprotection.

Main Methods:

  • Review of existing literature on NO signaling, mitochondrial function, and cardioprotection.
  • Analysis of studies demonstrating NO-induced posttranslational modifications of mitochondrial components, particularly Complex I.
  • Discussion of various pathways for inducing cardioprotective NO signaling, including NO-donors, nitrate/nitrite, and remote ischemic preconditioning (rIPC).

Main Results:

  • Hypoxic NO signaling in cardiomyocytes is linked to posttranslational modification of mitochondrial Complex I, reducing ROS burden.
  • NO-mediated cardioprotection involves intricate downstream signaling pathways within the cardiomyocyte.
  • Multiple strategies exist for inducing NO signaling, offering potential therapeutic avenues.

Conclusions:

  • NO signaling represents a significant endogenous cardioprotective mechanism against I/R injury.
  • Targeting mitochondrial posttranslational modifications offers a novel approach to NO-mediated cardioprotection.
  • Therapeutic induction of NO signaling holds promise for clinical application in preventing myocardial damage.
Keywords:
Ischemia/reperfusion injuryNO DonorNitrateNitric oxideNitriteS-nitrosation

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