ArticleJournal of molecular and cellular cardiology2010
Evidence that the acute phase of ischemic preconditioning does not require signaling by the A 2B adenosine receptor.
Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 30 citations in OpenAlex.
- Targeting myocardial equilibrative nucleoside transporter ENT1 provides cardioprotection by enhancing myeloid Adora2b signaling.JCI insight · 2023Article
- Adenosine and Adenosine Receptors: Advances in Atrial Fibrillation.Biomedicines · 2022Review
- The Hypoxia-Adenosine Link during Myocardial Ischemia-Reperfusion Injury.Biomedicines · 2022Review
- Review
- Decreased expression of adenosine receptor 2B confers cardiac protection against ischemia via restoring autophagic flux.American journal of translational research · 2020Article
- Cardioprotective role of APIP in myocardial infarction through ADORA2B.Cell death & disease · 2019Article
- Infarct-Sparing Effect of Adenosine A2B Receptor Agonist Is Primarily Due to Its Action on Splenic Leukocytes Via a PI3K/Akt/IL-10 Pathway.The Journal of surgical research · 2018Article
- Inhibition of tPA-induced hemorrhagic transformation involves adenosine A2b receptor activation after cerebral ischemia.Neurobiology of disease · 2017Article
- Purinergic regulation of the immune system.Nature reviews. Immunology · 2016Review
- The Many Faces of the A2b Adenosine Receptor in Cardiovascular and Metabolic Diseases.Journal of cellular physiology · 2015Review
- Adenosine 2B Receptor Activation Reduces Myocardial Reperfusion Injury by Promoting Anti-Inflammatory Macrophages Differentiation via PI3K/Akt Pathway.Oxidative medicine and cellular longevity · 2015Article
- Attenuating myocardial ischemia by targeting A2B adenosine receptors.Trends in molecular medicine · 2013Review
- Article
- Transgenic over expression of ectonucleotide triphosphate diphosphohydrolase-1 protects against murine myocardial ischemic injury.Journal of molecular and cellular cardiology · 2011Article
- A role for the low-affinity A2B adenosine receptor in regulating superoxide generation by murine neutrophils.The Journal of pharmacology and experimental therapeutics · 2011Article
- Adenosine A₂A and A₂B receptors are both required for adenosine A₁ receptor-mediated cardioprotection.American journal of physiology. Heart and circulatory physiology · 2011Article
- A2B adenosine receptors inhibit superoxide production from mitochondrial complex I in rabbit cardiomyocytes via a mechanism sensitive to Pertussis toxin.British journal of pharmacology · 2011Article
- Evidence for an intracellular localization of the adenosine A2B receptor in rat cardiomyocytes.Basic research in cardiology · 2011Article
- Role of adenosine A(2B) receptors in inflammation.Advances in pharmacology (San Diego, Calif.) · 2011Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Ischemic preconditioning (IPC) is a protective phenomenon in which brief ischemia renders the myocardium resistant to subsequent ischemic insults. Here, we used A(2B)AR gene knock-out (A(2B)KO)/β-galactosidase reporter gene knock-in mice and the A(2B)AR antagonist ATL-801 to investigate the potential involvement of the A(2B)AR in IPC, focusing on the acute phase of protection. Cardioprotection provided by acute IPC elicited by two 3-min occlusion/3-min reperfusion cycles was readily apparent in an isolated, Langendorff-perfused mouse heart model in studies using hearts from A(2B)KO mice. IPC equivalently improved the recovery of contractile function following 20 min of global ischemia and 45 min of reperfusion in both WT and A(2B)KO hearts by ~30-40%, and equivalently decreased the release of cardiac troponin I during the reperfusion period (from 5969 ± 925 to 1595 ± 674 ng/g and 4376 ± 739 to 2278 ± 462 ng/g using WT and A(2B)KO hearts, respectively). Similarly, the infarct size-reducing capacity of acute IPC in an in vivo model of infarction was fully manifested in experiments using A(2B)KO mice, as well as in experiments using rats pretreated with ATL-801. We did observe, however, a marked reduction in infarct size in rats following administration of the selective A(2B)AR agonist BAY 60-6583 (~25% reduction at a dose of 1.0mg/kg). While supportive of its concept as a cardioprotective receptor, these experiments indicate that the mechanism of the early phase of IPC is not dependent on signaling by the A(2B)AR. We present the idea that the A(2B)AR may contribute to the later stages of IPC dependent on the induction of stress-responsive genes.
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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.