ArticleESC heart failure2017
The neuroprotective agent Rasagiline mesylate attenuates cardiac remodeling after experimental myocardial infarction.
Article in ESC heart failure, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Article
- Not 'Inactive' After All: Cardiotoxic Mechanisms of Catecholamine Metabolism by Monoamine Oxidase.Cardiovascular toxicology · 2025Review
- Immunometabolism at the Heart of Cardiovascular Disease.JACC. Basic to translational science · 2023Review
- Importance of Mitochondria in Cardiac Pathologies: Focus on Uncoupling Proteins and Monoamine Oxidases.International journal of molecular sciences · 2023Review
- A new approach to sepsis treatment by rasagiline: a molecular, biochemical and histopathological study.Molecular biology reports · 2022Article
- Ubiquitin‑proteasomes are the dominant mediators of the regulatory effect of microRNA‑1 on cardiac remodeling after myocardial infarction.International journal of molecular medicine · 2019Article
- Polycaprolactone-based neurotherapeutic delivery of rasagiline targeting behavioral and biochemical deficits in Parkinson's disease.Drug delivery and translational research · 2019Article
- The neuroprotective agent Rasagiline mesylate attenuates cardiac remodeling after experimental myocardial infarction.ESC heart failure · 2017Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimRasagiline mesylate (N-propargyl-1 (R)-aminoindan) (RG) is a selective, potent irreversible inhibitor of monoamine oxidase-B with cardioprotective and anti-apoptotic properties. We investigated whether it could be cardioprotective in a rat model undergoing experimental myocardial infarction (MI) by permanent ligation of the left anterior descending coronary artery. METHODS AND
resultsRG was administered, intraperitoneally, for 28 days (2 mg/kg) starting 24 h after MI induction. Echocardiography analysis revealed a significant reduction in left ventricular end-systolic and diastolic dimensions and preserved fractional shortening in RG-treated compared with normal saline group at 28 days post-MI (31.6 ± 2.3 vs. 19.6 ± 1.8, P < 0.0001), respectively. Treatment with RG prevented tissue fibrosis as indicated by interstitial collagen estimation by immunofluorescence staining and hydroxyproline content and attenuated the number of apoptotic myocytes in the border zone (65%) as indicated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Caspase 3 relative protein levels were significantly decreased in the non-infarcted myocardium. Markedly decreased malondialdehyde levels in the border zone indicate a reduction in tissue oxidative stress.
conclusionsOur study demonstrates a positive effect of RG in the post-MI period with a significant attenuation in cardiac remodelling.
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