ArticleOxidative medicine and cellular longevity2015
Adenosine 2B Receptor Activation Reduces Myocardial Reperfusion Injury by Promoting Anti-Inflammatory Macrophages Differentiation via PI3K/Akt Pathway.
Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 57 citations in OpenAlex.
- Trial
- Metabolic regulation of myeloid-derived suppressor cells in tumor immune microenvironment: targets and therapeutic strategies.Theranostics · 2025Review
- Association of systemic inflammatory response index with ST segment elevation myocardial infarction and degree of coronary stenosis: a cross-sectional study.BMC cardiovascular disorders · 2024Article
- IL-6 in the infarcted heart is preferentially formed by fibroblasts and modulated by purinergic signaling.The Journal of clinical investigation · 2023Article
- Purinergic signaling in myocardial ischemia-reperfusion injury.Purinergic signalling · 2023Review
- Adenosine kinase promotes post-infarction cardiac repair by epigenetically maintaining reparative macrophage phenotype.Journal of molecular and cellular cardiology · 2023Article
- Activation of AExperimental and therapeutic medicine · 2022Article
- Extracellular vesicles derived from CD73 modified human umbilical cord mesenchymal stem cells ameliorate inflammation after spinal cord injury.Journal of nanobiotechnology · 2021Article
- Commentary: Planes, trains, and automobiles-Effective use of prolonged ex vivo heart preservation.Journal of cardiac surgery · 2021Article
- Role of Adenosine and Purinergic Receptors in Myocardial Infarction: Focus on Different Signal Transduction Pathways.Biomedicines · 2021Review
- Pharmacological Tuning of Adenosine Signal Nuances Underlying Heart Failure With Preserved Ejection Fraction.Frontiers in pharmacology · 2021Review
- Remote Conditioning by Rhythmic Compression of Limbs Ameliorated Myocardial Infarction by Downregulation of InflammationFrontiers in cardiovascular medicine · 2021Article
- Therapeutic Perspectives of Adenosine Deaminase Inhibition in Cardiovascular Diseases.Molecules (Basel, Switzerland) · 2020Review
- Review
- Extracellular nucleotide signaling in solid organ transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020Review
- Macrophage Activities in Myocardial Infarction and Heart Failure.Cardiology research and practice · 2020Review
- Non-Nucleoside Agonists of the Adenosine Receptors: An Overview.Pharmaceuticals (Basel, Switzerland) · 2019Review
- MicroRNA-32 targeting PTEN enhances M2 macrophage polarization in the glioma microenvironment and further promotes the progression of glioma.Molecular and cellular biochemistry · 2019Article
- Immune cells as targets for cardioprotection: new players and novel therapeutic opportunities.Cardiovascular research · 2019Review
- Regulation of Type 2 Immunity in Myocardial Infarction.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundActivation of the adenosine A2B receptor (A2BR) can reduce myocardial ischemia/reperfusion (IR) injury. However, the mechanism underlying the A2BR-mediated cardioprotection is less clear. The present study was designed to investigate the potential mechanisms of cardioprotection mediated by A2BR. METHODS AND
resultsC57BL/6 mice underwent 40-minute ischemia and 60-minute reperfusion. ATL-801, a potent selective A2BR antagonist, could not block ischemic preconditioning induced protection. BAY 60-6583, a highly selective A2BR agonist, significantly reduced myocardial infarct size, and its protective effect could be blocked by either ATL-801 or wortmannin. BAY 60-6583 increased phosphorylated Akt (p-Akt) levels in the heart at 10 min of reperfusion, and this phosphorylation could also be blocked by ATL-801 or wortmannin. Furthermore, BAY 60-6583 significantly increased M2 macrophages and decreased M1 macrophage and neutrophils infiltration in reperfused hearts, which also could be blocked by wortmannin. Meanwhile, confocal imaging studies showed that the majority of Akt phosphorylation in the heart was colocalized to CD206+ cells in both control and BAY 60-6583 pretreated hearts.
conclusionOur results indicated that pretreatment with BAY 60-6583 protects the heart against myocardial IR injury by its anti-inflammatory effects, probably by modulating macrophages phenotype switching via a PI3K/Akt pathway.
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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.