title: Monoamine oxidases (MAO) in the pathogenesis of heart failure and ischemia/reperfusion injury.
abstract: Recent evidence highlights monoamine oxidases (MAO) as another prominent source of oxidative stress. MAO are a class of enzymes located in the outer mitochondrial membrane, deputed to the oxidative breakdown of key neurotransmitters such as norepinephrine, epinephrine and dopamine, and in the process generate H(2)O(2). All these monoamines are endowed with potent modulatory effects on myocardial function. Thus, when the heart is subjected to chronic neuro-hormonal and/or peripheral hemodynamic stress, the abundance of circulating/tissue monoamines can make MAO-derived H(2)O(2) production particularly prominent. This is the case of acute cardiac damage due to ischemia/reperfusion injury or, on a more chronic stand, of the transition from compensated hypertrophy to overt ventricular dilation/pump failure. Here, we will first briefly discuss mitochondrial status and contribution to acute and chronic cardiac disorders. We will illustrate possible mechanisms by which MAO activity affects cardiac biology and function, along with a discussion as to their role as a prominent source of reactive oxygen species. Finally, we will speculate on why MAO inhibition might have a therapeutic value for treating cardiac affections of ischemic and non-ischemic origin. This article is part of a Special Issue entitled: Mitochondria and Cardioprotection.
authors.affiliation: Department of Biomedical Sciences, University of Padova, viale G. Colombo 3, 35121 Padova, Italy. nina.kaludercic@unipd.it
authors.forename: Nina
authors.initials: N
authors.lastname: Kaludercic
authors.forename: Andrea
authors.initials: A
authors.lastname: Carpi
authors.forename: Roberta
authors.initials: R
authors.lastname: Menabò
authors.forename: Fabio
authors.initials: F
authors.lastname: Di Lisa
authors.forename: Nazareno
authors.initials: N
authors.lastname: Paolocci
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000188:drug therapy / Q000378:metabolism; D055786:Gene Knockout Techniques; D006333:Heart Failure / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D051379:Mice; D008929:Mitochondria, Heart / Q000378:metabolism*; D008995:Monoamine Oxidase / Q000235:genetics / Q000378:metabolism*; D008996:Monoamine Oxidase Inhibitors / Q000627:therapeutic use; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D018377:Neurotransmitter Agents / Q000378:metabolism; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D008996:Monoamine Oxidase Inhibitors; D018377:Neurotransmitter Agents; D017382:Reactive Oxygen Species; D008995:Monoamine Oxidase