Acute inhibition of monoamine oxidase and ischemic preconditioning in isolated rat hearts: interference with postischemic functional recovery but no effect on infarct size reduction

Dănilă, Mirela; Privistirescu, Andreea; Mirica, Silvia Nicoleta; Sturza, Adrian; Ordodi, Valentin; Noveanu, Lavinia; Duicu, Oana; Muntean, Daniela-Lucia

doi:10.1139/cjpp-2015-0103

Cited by 6 publications

(2 citation statements)

References 46 publications

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“…Supporting this claim, MAO inhibition in the settings of IPC has been reported to abolish cardioprotection (Di Lisa, unpublished observations, cited by [ 213 ]). However, in a recent study in isolated rat hearts subjected to a preconditioning protocol, we have demonstrated that bracketing the IPC episodes with MAO inhibitors did not interfere with the antinecrotic protection but potentiated the postischaemic functional recovery [ 214 ].…”

Section: Mitochondria As Sources Of Beneficial Rosmentioning

confidence: 99%

The Role of Mitochondrial Reactive Oxygen Species in Cardiovascular Injury and Protective Strategies

Muntean¹,

Sturza²,

Dănilă³

et al. 2016

Oxidative Medicine and Cellular Longevity

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Ischaemia/reperfusion (I/R) injury of the heart represents a major health burden mainly associated with acute coronary syndromes. While timely coronary reperfusion has become the established routine therapy in patients with ST-elevation myocardial infarction, the restoration of blood flow into the previously ischaemic area is always accompanied by myocardial injury. The central mechanism involved in this phenomenon is represented by the excessive generation of reactive oxygen species (ROS). Besides their harmful role when highly generated during early reperfusion, minimal ROS formation during ischaemia and/or at reperfusion is critical for the redox signaling of cardioprotection. In the past decades, mitochondria have emerged as the major source of ROS as well as a critical target for cardioprotective strategies at reperfusion. Mitochondria dysfunction associated with I/R myocardial injury is further described and ultimately analyzed with respect to its role as source of both deleterious and beneficial ROS. Furthermore, the contribution of ROS in the highly investigated field of conditioning strategies is analyzed. In the end, the vascular sources of mitochondria-derived ROS are briefly reviewed.

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Section: Mitochondria As Sources Of Beneficial Rosmentioning

confidence: 99%

The Role of Mitochondrial Reactive Oxygen Species in Cardiovascular Injury and Protective Strategies

Muntean¹,

Sturza²,

Dănilă³

et al. 2016

Oxidative Medicine and Cellular Longevity

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“…In both male and female rat hearts, ischemic preconditioning improves functional recovery following I/R, which is further enhanced in the presence of MAO inhibition by either clorgyline or pargyline. However, infarct size is similar among all preconditioned groups, regardless of the presence of MAO inhibitors, indicating that acute inhibition of MAOs potentiates the preconditioning-induced postischemic functional recovery without having any further effect on infarct size beyond that achieved by ischemic preconditioning [ 177 ].…”

Section: Monoamine Oxidases (Mao)mentioning

confidence: 99%

Importance of Mitochondria in Cardiac Pathologies: Focus on Uncoupling Proteins and Monoamine Oxidases

Schulz

Schlüter

2023

IJMS

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On the one hand, reactive oxygen species (ROS) are involved in the onset and progression of a wide array of diseases. On the other hand, these are a part of signaling pathways related to cell metabolism, growth and survival. While ROS are produced at various cellular sites, in cardiomyocytes the largest amount of ROS is generated by mitochondria. Apart from the electron transport chain and various other proteins, uncoupling protein (UCP) and monoamine oxidases (MAO) have been proposed to modify mitochondrial ROS formation. Here, we review the recent information on UCP and MAO in cardiac injuries induced by ischemia-reperfusion (I/R) as well as protection from I/R and heart failure secondary to I/R injury or pressure overload. The current data in the literature suggest that I/R will preferentially upregulate UCP2 in cardiac tissue but not UCP3. Studies addressing the consequences of such induction are currently inconclusive because the precise function of UCP2 in cardiac tissue is not well understood, and tissue- and species-specific aspects complicate the situation. In general, UCP2 may reduce oxidative stress by mild uncoupling and both UCP2 and UCP3 affect substrate utilization in cardiac tissue, thereby modifying post-ischemic remodeling. MAOs are important for the physiological regulation of substrate concentrations. Upon increased expression and or activity of MAOs, however, the increased production of ROS and reactive aldehydes contribute to cardiac alterations such as hypertrophy, inflammation, irreversible cardiomyocyte injury, and failure.

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β-Adrenergic signaling, monoamine oxidase A and antioxidant defence in the myocardium of SHR and SHR-mtBN conplastic rat strains: the effect of chronic hypoxia

et al. 2017

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The β-adrenergic signaling pathways and antioxidant defence mechanisms play important roles in maintaining proper heart function. Here, we examined the effect of chronic normobaric hypoxia (CNH, 10% O, 3 weeks) on myocardial β-adrenergic signaling and selected components of the antioxidant system in spontaneously hypertensive rats (SHR) and in a conplastic SHR-mtBN strain characterized by the selective replacement of the mitochondrial genome of SHR with that of the more ischemia-resistant Brown Norway strain. Our investigations revealed some intriguing differences between the two strains at the level of β-adrenergic receptors (β-ARs), activity of adenylyl cyclase (AC) and monoamine oxidase A (MAO-A), as well as distinct changes after CNH exposure. The β-AR/β-AR ratio was significantly higher in SHR-mtBN than in SHR, apparently due to increased expression of β-ARs. Adaptation to hypoxia elevated β-ARs in SHR and decreased the total number of β-ARs in SHR-mtBN. In parallel, the ability of isoprenaline to stimulate AC activity was found to be higher in SHR-mtBN than that in SHR. Interestingly, the activity of MAO-A was notably lower in SHR-mtBN than in SHR, and it was markedly elevated in both strains after exposure to hypoxia. In addition to that, CNH markedly enhanced the expression of catalase and aldehyde dehydrogenase-2 in both strains, and decreased the expression of Cu/Zn superoxide dismutase in SHR. Adaptation to CNH intensified oxidative stress to a similar extent in both strains and elevated the IL-10/TNF-α ratio in SHR-mtBN only. These data indicate that alterations in the mitochondrial genome can result in peculiar changes in myocardial β-adrenergic signaling, MAO-A activity and antioxidant defence and may, thus, affect the adaptive responses to hypoxia.

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Acute inhibition of monoamine oxidase and ischemic preconditioning in isolated rat hearts: interference with postischemic functional recovery but no effect on infarct size reduction

Cited by 6 publications

References 46 publications

The Role of Mitochondrial Reactive Oxygen Species in Cardiovascular Injury and Protective Strategies

The Role of Mitochondrial Reactive Oxygen Species in Cardiovascular Injury and Protective Strategies

Importance of Mitochondria in Cardiac Pathologies: Focus on Uncoupling Proteins and Monoamine Oxidases

β-Adrenergic signaling, monoamine oxidase A and antioxidant defence in the myocardium of SHR and SHR-mtBN conplastic rat strains: the effect of chronic hypoxia

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