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Oxidative Medicine and Cellular Longevity
Volume 2016 (2016), Article ID 4375418, 10 pages
Research Article

Monoamine Oxidase Is Overactivated in Left and Right Ventricles from Ischemic Hearts: An Intriguing Therapeutic Target

1Department of Neurosciences, Psychology, Drug Research and Child Health (NEUROFARBA), Center of Molecular Medicine (CIMMBA), University of Florence, Florence, Italy
2Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy
3Department of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome, Rome, Italy

Received 12 July 2016; Revised 19 September 2016; Accepted 9 October 2016

Academic Editor: Mohammad T. Elnakish

Copyright © 2016 Maria Elena Manni et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Growing evidence indicates that reactive oxygen species (ROS) may play a key role in human heart failure (HF). Monoamine oxidase (MAO) is emerging as a major ROS source in several cardiomyopathies. However, little is known about MAO activity in human failing heart and its relationship with redox imbalance. Therefore, we measured MAO activity in the left (LV) and in the right (RV) ventricle of human nonfailing (NF) and in end-stage ischemic (IHD) and nonischemic failing hearts. We found that both MAO isoforms (MAO-A/B) significantly increased in terms of activity and expression levels only in IHD ventricles. Catalase and aldehyde dehydrogenase-2 activities (ALDH-2), both implicated in MAO-catalyzed catecholamine catabolism, were significantly elevated in the failing LV, whereas, in the RV, statistical significance was observed only for ALDH-2. Oxidative stress markers levels were significantly increased only in the failing RV. Actin oxidation was significantly elevated in both failing ventricles and related to MAO-A activity and to functional parameters. These data suggest a close association between MAO-A-dependent ROS generation, actin oxidation, and ventricular dysfunction. This latter finding points to a possible pathogenic role of MAO-A in human myocardial failure supporting the idea that MAO-A could be a new therapeutic target in HF.