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Monoamine oxidases as sources of oxidants in the heart

Nina Kaludercic1, Jeanne Mialet-Perez2, Nazareno Paolocci3

  • 1Neuroscience Institute, National Research Council of Italy (CNR), Padua, Italy.

Journal of Molecular and Cellular Cardiology
|January 14, 2014
PubMed

Insights

Monoamine oxidase (MAO) contributes to oxidative stress in the heart by producing harmful byproducts. Inhibiting MAO may offer cardiovascular benefits, but its precise role requires further study.

Area of Science:

  • Mitochondrial biochemistry
  • Cardiovascular pathophysiology
  • Redox signaling

Background:

  • Mitochondria are key sites of oxidative stress.
  • Monoamine oxidase (MAO) is a significant mitochondrial source of reactive oxygen species.
  • MAO activity impacts cardiac function and viability through H2O2 and aldehyde generation.

Purpose of the Study:

  • To review the role of MAO in catecholamine and serotonin metabolism within the cardiovascular system.
  • To discuss the contribution of MAO isoforms (MAO-A and MAO-B) to mitochondrial dysfunction and myocardial injury.
  • To examine the therapeutic potential and adverse effects of MAO modulation in the heart.

Main Methods:

  • Review of existing literature on MAO function in the cardiovascular system.
  • Analysis of MAO isoform-specific roles in mitochondrial dysfunction.
  • Evaluation of pharmacological and genetic inhibition/overexpression studies.

Main Results:

  • MAO activity generates reactive oxygen species and aldehydes impacting cardiac mitochondria.
  • Both MAO-A and MAO-B contribute to myocardial injury.
  • MAO inhibition shows potential benefits, while MAO knockout mice exhibit baseline adverse effects.

Conclusions:

  • MAO plays a critical role in cardiac oxidative stress and pathophysiology.
  • Targeting MAO offers potential therapeutic strategies for cardiovascular diseases.
  • Further research is needed to fully understand MAO's complex role and optimize therapeutic interventions.
Keywords:
Heart failureIschemia/reperfusion injuryMitochondrial dysfunctionMonoamine oxidaseOxidative stress

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