ArticleBiochemical pharmacology2006
Uridine-5'-triphosphate (UTP) reduces infarct size and improves rat heart function after myocardial infarct.
Article in Biochemical pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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Who cites it
18 citing papers in PubMed, 54 citations in OpenAlex.
- Crosstalk among Reactive Oxygen Species, Autophagy and Metabolism in Myocardial Ischemia and Reperfusion Stages.Aging and disease · 2024Review
- Stimulation of P2Y11 receptor protects human cardiomyocytes against Hypoxia/Reoxygenation injury and involves PKCε signaling pathway.Scientific reports · 2019Article
- On inotropic effects of UTP in the human heart.Heliyon · 2019Review
- Dynamic Sampling and Information Encoding in Biochemical Networks.Biophysical journal · 2017Article
- Loss of Mouse P2Y6 Nucleotide Receptor Is Associated with Physiological Macrocardia and Amplified Pathological Cardiac Hypertrophy.The Journal of biological chemistry · 2016Article
- Cardiac purinergic signalling in health and disease.Purinergic signalling · 2015Review
- Adenosine diphosphate reduces infarct size and improves porcine heart function after myocardial infarct.Physiological reports · 2013Article
- Spatial-temporal dynamics of collective chemosensing.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Cardiomyocyte death induced by ischaemic/hypoxic stress is differentially affected by distinct purinergic P2 receptors.Journal of cellular and molecular medicine · 2012Article
- Anti-ischemic effects of multivalent dendrimeric A₃ adenosine receptor agonists in cultured cardiomyocytes and in the isolated rat heart.Pharmacological research · 2012Article
- Uridine triphosphate (UTP) induces profibrotic responses in cardiac fibroblasts by activation of P2Y2 receptors.Journal of molecular and cellular cardiology · 2010Article
- Autophagy induced by ischemic preconditioning is essential for cardioprotection.Journal of cardiovascular translational research · 2010Article
- P2Y nucleotide receptors: promise of therapeutic applications.Drug discovery today · 2010Review
- Characterization of P2Y receptor subtypes functionally expressed on neonatal rat cardiac myofibroblasts.British journal of pharmacology · 2009Article
- Involvement of UTP in protection of cardiomyocytes from hypoxic stress.Canadian journal of physiology and pharmacology · 2009Article
- Opposite effects of uracil and adenine nucleotides on the survival of murine cardiomyocytes.Journal of cellular and molecular medicine · 2008Article
- P2 receptors in cardiovascular regulation and disease.Purinergic signalling · 2008Article
- Increased O-GlcNAc levels during reperfusion lead to improved functional recovery and reduced calpain proteolysis.American journal of physiology. Heart and circulatory physiology · 2007Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
We have previously found that uridine 5'-triphosphate (UTP) significantly reduced cardiomyocyte death induced by hypoxia via activating P2Y(2) receptors. To explore the effect of UTP following myocardial infarction (MI) in vivo we studied four groups: sham with or without LAD ligation, injected with UTP (0.44microg/kg i.v.) 30min before MI, and UTP injection (4.4microg/kg i.v.) 24h prior to MI. Left ventricular end diastolic area (LVEDA), end systolic area (LVESA) fractional shortening (FS), and changes in posterior wall (PW) thickness were performed by echocardiography before and 24h after MI. In addition, we measured different biochemical markers of damage and infarct size using Evans blue and TTC staining. The increase in LVEDA and LVESA of the treated animals was significantly smaller when compared to the MI rats (p<0.01). Concomitantly, FS was higher in groups pretreated with UTP 30min or 24h (56+/-14.3 and 36.7+/-8.2%, p<0.01, respectively). Ratio of infarct size to area at risk was smaller in the UTP pretreated hearts than MI rats (22.9+/-6.6, 23.1+/-9.1%, versus 45.4+/-7.6%, respectively, p<0.001). Troponin T and ATP measurements, demonstrated reduced myocardial damage. Using Rhod-2-AM loaded cardiomyocytes, we found that UTP reduced mitochondrial calcium levels following hypoxia. In conclusion, early or late UTP preconditioning is effective, demonstrating reduced infarct size and superior myocardial function. The resulting cardioprotection following UTP treatment post ischemia demonstrates a reduction in mitochondrial calcium overload, which can explain the beneficial effect of UTP.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.