Oxidative Stress by Monoamine Oxidase-A Impairs Transcription Factor EB Activation and Autophagosome Clearance, Leading to Cardiomyocyte Necrosis and Heart Failure

2016 ◽  
Vol 25 (1) ◽  
pp. 10-27 ◽  
Author(s):  
Yohan Santin ◽  
Pierre Sicard ◽  
François Vigneron ◽  
Céline Guilbeau-Frugier ◽  
Marianne Dutaur ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Transcription Factor ◽  
Monoamine Oxidase ◽  
Monoamine Oxidase A ◽  
Transcription Factor Eb

Monoamine Oxidase A Contributes to Oxidative Stress and Is Associated with Development of Diabetic Cardiomyopathy

2015 ◽  
Vol 87 ◽  
pp. S27-S28
Author(s):  
Prachi Umbarkar ◽  
Sarojini Singh ◽  
Silpa Arkat ◽  
S.L. Bodhankar ◽  
Sathiyanarayanan Lohidasan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Monoamine Oxidase ◽  
Diabetic Cardiomyopathy ◽  
Monoamine Oxidase A

scholarly journals Regulation of central angiotensin type 1 receptors and sympathetic outflow in heart failure

2009 ◽  
Vol 297 (5) ◽  
pp. H1557-H1566 ◽  
Author(s):  
Irving H. Zucker ◽  
Harold D. Schultz ◽  
Kaushik P. Patel ◽  
Wei Wang ◽  
Lie Gao
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Transcription Factor ◽  
Critical Role ◽  
Good Evidence ◽  
Receptor Expression ◽  
Ventrolateral Medulla ◽  
Sympathetic Outflow ◽  
Angiotensin Type

Angiotensin type 1 receptors (AT1Rs) play a critical role in a variety of physiological functions and pathophysiological states. They have been strongly implicated in the modulation of sympathetic outflow in the brain. An understanding of the mechanisms by which AT1Rs are regulated in a variety of disease states that are characterized by sympathoexcitation is pivotal in development of new strategies for the treatment of these disorders. This review concentrates on several aspects of AT1R regulation in the setting of chronic heart failure (CHF). There is now good evidence that AT1R expression in neurons is mediated by activation of the transcription factor activator protein 1 (AP-1). This transcription factor and its component proteins are upregulated in the rostral ventrolateral medulla of animals with CHF. Because the increase in AT1R expression and transcription factor activation can be blocked by the AT1R antagonist losartan, a positive feedback mechanism of AT1R expression in CHF is suggested. Oxidative stress has also been implicated in the regulation of receptor expression. Recent data suggest that the newly discovered catabolic enzyme angiotensin-converting enzyme 2 (ACE2) may play a role in the modulation of AT1R expression by altering the balance between the octapeptide ANG II and ANG- (1–7). Finally, exercise training reduces both central oxidative stress and AT1R expression in animals with CHF. These data strongly suggest that multiple central and peripheral influences dynamically alter AT1R expression in CHF.

Brain monoamine oxidase A in hyperammonemia is regulated by NMDA receptors

2009 ◽  
Vol 4 (3) ◽  
pp. 321-326
Author(s):  
Elena Kosenko ◽  
Yury Kaminsky
Keyword(s):  
Oxidative Stress ◽  
Nmda Receptor ◽  
Monoamine Oxidase ◽  
Nmda Receptors ◽  
Monoamine Oxidase A ◽  
Mk 801 ◽  
Mao A ◽  
Vitro Effect

AbstractMitochondrial enzyme monoamine oxidase A (MAO-A) generates hydrogen peroxide (H2O2) and is up-regulated by Ca2+ and presumably by ammonia. We hypothesized that MAO-A may be under the control of NMDA receptors in hyperammonemia. In this work, the in vivo effects of single dosing with ammonia and NMDA receptor antagonist MK-801 and the in vitro effect of Ca2+ on MAO-A activity in isolated rat brain mitochondria were studied employing enzymatic procedure. Intraperitoneal injection of rats with ammonia led to an increase in MAO-A activity in mitochondria indicating excessive H2O2 generation. Calcium added to isolated mitochondria stimulated MAO-A activity by as much as 84%. MK-801 prevented the in vivo effect of ammonia, implying that MAO-A activation in hyperammonemia is mediated by NMDA receptors. These data support the conclusion that brain mitochondrial MAO-A is regulated by the function of NMDA receptors. The enzyme can contribute to the oxidative stress associated with hyperammonemic conditions such as encephalopathy and Alzheimer’s disease. The attenuation of the oxidative stress highlights MAO-A inactivation and NMDA receptor antagonists as sources of novel avenues in the treatment of mental disorders.

Inhibition of Monoamine Oxidase A in pulmonary artery banding-induced right heart failure

2019 ◽  
Author(s):  
Eva Peters ◽  
Xiaoqing Sun ◽  
Stine Andersen ◽  
Julie Birkmose Axelsen ◽  
Ingrid Schalij ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Artery ◽  
Monoamine Oxidase ◽  
Right Heart Failure ◽  
Monoamine Oxidase A ◽  
Pulmonary Artery Banding ◽  
Right Heart

scholarly journals Oxidative Stress–Dependent Sphingosine Kinase-1 Inhibition Mediates Monoamine Oxidase A–Associated Cardiac Cell Apoptosis

2007 ◽  
Vol 100 (1) ◽  
pp. 41-49 ◽  
Author(s):  
Dimitri Pchejetski ◽  
Oxana Kunduzova ◽  
Audrey Dayon ◽  
Denis Calise ◽  
Marie-Hélène Seguelas ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Monoamine Oxidase ◽  
Cell Apoptosis ◽  
Sphingosine Kinase ◽  
Monoamine Oxidase A ◽  
Cardiac Cell ◽  
Sphingosine Kinase 1 ◽  
Stress Dependent
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