The neuroprotective agent Rasagiline mesylate attenuates cardiac remodeling after experimental myocardial infarction

Varela, Aimilia; Mavroidis, Manolis; Katsimpoulas, Michalis; Sfiroera, Irini; Kappa, Niki; Mesa, Angelica; Kostomitsopoulos, Nikolaos; Cokkinos, Dennis V.

doi:10.1002/ehf2.12140

Cited by 9 publications

(5 citation statements)

References 42 publications

(90 reference statements)

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“…have been reported with the use of rasagiline in the post-MI rat. 56 Thyroid hormones increase alpha-MHC, SERCA-2 and decrease apoptosis; studies have shown that thyroid supplementation in the animal prevents or reverses REM. 20,57,58 Around 30 % of patients with congestive heart failure have low triiodothyronine (T3) levels, constituting the 'low T3 syndrome'.…”

Section: Novel Drugs and Therapiesmentioning

confidence: 99%

Left Ventricular Remodelling: A Problem in Search of Solutions

Cokkinos

Belogianneas

2016

European Cardiology Review

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Cardiac remodelling (REM) is a generally unfavourable process that leads to left ventricular dilation in response to cardiac injury, predominantly acute myocardial infarction (AMI). REM occurs in around 30 % of anterior infarcts despite timely primary coronary intervention and the use of drugs, i.e. angiotensin-converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARBs), betablockers, aldosterone inhibitors and statins. In order to diagnose REM, many imaging modalities (echocardiography, cardiac magnetic resonance, scintigraphy) are employed together with an increasing number of serum biomarkers including microRNAs. The most widely used definition of REM is a >20 % increase in left ventricular end-diastolic volume (LVEDV). There is also evidence that regression of REM can occur, i.e. reverse REM. The latter is defined as a ≥10 % decrease in left ventricular end-systolic volume (LVESV) and confers a more favourable outcome. Many therapeutic agents may be used during primary intervention and over the long term; however, few have demonstrated significant benefits. Revascularisation, anti-REM surgery and, where indicated, cardiac resynchronisation therapy can be of benefit. Gene therapy by sarcoplasmic reticulum Ca2+ ATPase 2 (SERCA-2a) transfer has been investigated but data from the Calcium upregulation by percutaneous administration of gene therapy in patients with cardiac disease (CUPID 2) trial were disappointing. Progenitor cell therapy shows promise. In conclusion, therapy for REM remains inadequate.

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Section: Novel Drugs and Therapiesmentioning

confidence: 99%

Left Ventricular Remodelling: A Problem in Search of Solutions

Cokkinos

Belogianneas

2016

European Cardiology Review

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“…In the experimental MI model, it has been shown that rasagiline administration reduces oxidative stress, and consequently tissue MDA levels decrease. [14]Carrilo et al…”

Section: Discussionmentioning

confidence: 99%

“…[13]Varela et al demonstrated the cardioprotective effects of rasagiline in the experimental myocardial infarction model. [14]In this case, it is thought that rasagiline may have effects on peripheral diseases besides its effects on central diseases.…”

Section: Introductionmentioning

confidence: 99%

A new approach to sepsis treatment by rasagiline: a molecular, biochemical and histopathological study

Uğan

Köse

et al. 2022

Mol Biol Rep

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Aim:We aimed to investigate the effects of rasagiline, which has a strong antioxidant, anti-apoptotic and anti-in ammatory effect, on acute lung injury that develops in the sepsis model induced with the CLP in rats.Main Methods:The rats were separated into the following six groups, Group 1: Sham, Group 2: Sham + Rasegiline 4 mg/kg, Group 3: Sepsis, Group 4: Sepsis + Rasegiline 1 mg/kg, Group 5: Sepsis + Rasegiline 2 mg/kg, Group 6: Sepsis + Rasegiline 4 mg/kg. A total of 4 holes were opened with a 16-gauge needle through the cecum distal to the point of ligation.Key Findings:GSH levels appear to improve due to increased doses of rasagiline, while SOD activity appears to improve only at the high dose of rasagiline. There was a statistically signi cant improvement in the doses of R2 and R4. This improvement in Tnf-α, IL1β, IL6, NF-κβand HMGB1 expression increased dose-dependent at R2 and R4 doses. In increased doses, rasagiline appears to prevent the development of edema, the formation of in ammation, and hemorrhagic areas are almost similar to healthy tissue.Signi cance: Rasagiline exerts both antioxidant and anti-in ammatory effects on CLP induced acute lung injury in rats.

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“…Rasagiline mesylate (N-propargyl-1 (R)-aminoindan) (RG), a selective, potent irreversible inhibitor of monoamine oxidase-B, administered for 28 days (2 mg/kg) starting 24 h after myocardial infarction, preserves left ventricular geometry and function. Treatment with rasagiline prevents tissue fibrosis and attenuates cardiomyocyte apoptosis in the border zone of the infarct associated with a markedly-decreased malondialdehyde level in the border zone, indicating a reduction in tissue oxidative stress [ 178 ]. Additionally, MAO-A is an important source of oxidative stress in the heart and MAO-A-derived reactive oxygen species contribute to dilated cardiomyopathy [ 145 ].…”

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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The neuroprotective agent Rasagiline mesylate attenuates cardiac remodeling after experimental myocardial infarction

Cited by 9 publications

References 42 publications

Left Ventricular Remodelling: A Problem in Search of Solutions

Left Ventricular Remodelling: A Problem in Search of Solutions

A new approach to sepsis treatment by rasagiline: a molecular, biochemical and histopathological study

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

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