ArticleJournal of molecular and cellular cardiology2001
Activation of A(3)adenosine receptor protects against doxorubicin-induced cardiotoxicity.
Article in Journal of molecular and cellular cardiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 74 citations in OpenAlex.
- A3 Adenosine Receptor Agonists as Multisystem Disease Modifiers: From Molecular Signaling to Clinical Translation.Biomolecules · 2026Review
- Class Effect of SGLT2 Inhibitors Against Doxorubicin-Induced Cardiotoxicity via Regulating Adenosine Kinase Mediated-Cardiac Oxidative Stress.Cardiovascular drugs and therapy · 2026Article
- Adenosine AInternational journal of molecular sciences · 2024Review
- MD-1 Deficiency Accelerates Myocardial Inflammation and Apoptosis in Doxorubicin-Induced Cardiotoxicity by Activating the TLR4/MAPKs/Nuclear Factor kappa B (NF-κB) Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Targeting GPCRs Against Cardiotoxicity Induced by Anticancer Treatments.Frontiers in cardiovascular medicine · 2019Review
- The Polymorphism inBioMed research international · 2018Article
- Identification of A3 adenosine receptor agonists as novel non-narcotic analgesics.British journal of pharmacology · 2016Review
- The role of mutant protein level in autosomal recessive catecholamine dependent polymorphic ventricular tachycardia (CPVT2).Biochemical pharmacology · 2013Article
- Pharmacological and therapeutic effects of A3 adenosine receptor agonists.Drug discovery today · 2012Review
- Predicted structures of agonist and antagonist bound complexes of adenosine A3 receptor.Proteins · 2011Article
- TVP1022 protects neonatal rat ventricular myocytes against doxorubicin-induced functional derangements.The Journal of pharmacology and experimental therapeutics · 2010Article
- Involvement of UTP in protection of cardiomyocytes from hypoxic stress.Canadian journal of physiology and pharmacology · 2009Article
- Medicinal chemistry of the A3 adenosine receptor: agonists, antagonists, and receptor engineering.Handbook of experimental pharmacology · 2009Review
- Adenosine A3 receptor deficiency exerts unanticipated protective effects on the pressure-overloaded left ventricle.Circulation · 2008Article
- Article
- Modulation of the Akt/Ras/Raf/MEK/ERK pathway by A₃ adenosine receptor.Purinergic signalling · 2006Article
- Adenosine receptors as therapeutic targets.Nature reviews. Drug discovery · 2006Review
- Delta-9-tetrahydrocannabinol protects cardiac cells from hypoxia via CB2 receptor activation and nitric oxide production.Molecular and cellular biochemistry · 2006Article
- Action of nucleosides and nucleotides at 7 transmembrane-spanning receptors.Nucleosides, nucleotides & nucleic acids · 2006Review
- Role of adenosine A1 and A3 receptors in regulation of cardiomyocyte homeostasis after mitochondrial respiratory chain injury.American journal of physiology. Heart and circulatory physiology · 2005Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Adenosine exerts a marked protective effect on the heart during cardiac ischemia. This protection is mediated by binding to the A(1)and A(3)subtypes of adenosine receptor (A(1)R and A(3)R, respectively). The objective of the present study was to investigate whether activation of A(1)and A(3)adenosine receptors may reduce doxorubicin-induced damage to cardiomyocytes in culture. Cultured cardiomyocytes from newborn rats were treated with 0.5--5 microm doxorubicin (DOX) for 18 h and then incubated in drug-free medium for an additional 24 h. This treatment resulted in cell damage and lactate dehydrogenase release, even after low (0.5 microm) doses of the drug, and increased in a concentration-dependent manner. Activation of A(3)-subtype but not A(1)-subtype receptors attenuated doxorubicin-cardiotoxicity after drug treatment for 18 h followed by 24 h incubation in drug-free medium. Modulation of intracellular calcium mediated by activation of A(3)R, but not by A(1)R, in cultured myocytes suggested an important pathophysiological significance of this subtype of adenosine receptors. Protection by A(3)R agonist Cl-IB-MECA (2-chloro-N(6)-(3-iodobenzyl)adenosine-5'-N-methyluronamide) following DOX treatment is evident in: (1) decreases in intracellular calcium overloading and abnormalities in Ca(2+)transients; (2) reduction of free-radical generation and lipid peroxidation; (3) attenuation of mitochondrial damage by protection of the terminal link (COX-complex) of respiratory chain; (4) attenuation of the decrease in ATP production and irreversible cardiomyocyte damage. Cardioprotection caused by Cl-IB-MECA was antagonized considerably by the selective A(3)adenosine receptor antagonist MRS1523.
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Registered trials
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.