ArticleProceedings of the National Academy of Sciences of the United States of America2007
A1 adenosine receptors play an essential role in protecting the embryo against hypoxia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- ENT1 inhibition links oligodendrocyte lipid metabolism to connectivity in tauopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Insights from animal models: Dissecting the independent roles of oxygen and nutrients in the fetal origins of cardiovascular disease.The Journal of physiology · 2026Review
- Caffeine as a Treatment for Perinatal Hypoxic-Ischemic Brain Injury: The Potential Risks and Benefits.Developmental neuroscience · 2026Review
- Prenatal Hypoxia Affects Foetal Cardiovascular Regulatory Mechanisms in a Sex- and Circadian-Dependent Manner: A Review.International journal of molecular sciences · 2022Review
- Advances in protein misfolding, amyloidosis and its correlation with human diseases.3 Biotech · 2020Review
- Long-term consequences of disrupting adenosine signaling during embryonic development.Molecular aspects of medicine · 2017Review
- A hypoxic episode during cardiogenesis downregulates the adenosinergic system and alters the myocardial anoxic tolerance.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
- Effect of Caffeine Chronically Consumed During Pregnancy on Adenosine AJournal of caffeine research · 2014Article
- Embryonic caffeine exposure acts via A1 adenosine receptors to alter adult cardiac function and DNA methylation in mice.PloS one · 2014Article
- Regulation of cardiovascular development by adenosine and adenosine-mediated embryo protection.Arteriosclerosis, thrombosis, and vascular biology · 2012Review
- Adenosine A₂a receptors and O₂ sensing in development.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Review
- The Sphingosine-1-phospate receptor 1 mediates S1P action during cardiac development.BMC developmental biology · 2011Article
- Bioenergetics, mitochondria, and cardiac myocyte differentiation.Progress in pediatric cardiology · 2011Article
- Adverse and protective influences of adenosine on the newborn and embryo: implications for preterm white matter injury and embryo protection.Pediatric research · 2011Review
- International Union of Basic and Clinical Pharmacology. LXXXI. Nomenclature and classification of adenosine receptors--an update.Pharmacological reviews · 2011Review
- Article
- Effects of maternal hypoxia on muscle vasodilatation evoked by acute systemic hypoxia in adult rat offspring: changed roles of adenosine and A1 receptors.The Journal of physiology · 2010Article
- Identification of the heart as the critical site of adenosine mediated embryo protection.BMC developmental biology · 2010Article
- Article
- Regulation of cerebrospinal fluid production by caffeine consumption.BMC neuroscience · 2009Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Embryos can be exposed to environmental factors that induce hypoxia. Currently, our understanding of the effects of hypoxia on early mammalian development is modest. Potential mediators of hypoxia action include the nucleoside adenosine, which acts through A(1) adenosine receptors (A(1)ARs) and mediates adverse effects of hypoxia on the neonatal brain. We hypothesized that A(1)ARs may also play a role in mediating effects of hypoxia on the embryo. When pregnant dams were exposed to hypoxia (10% O(2)) beginning at embryonic day (E) 7.5 or 8.5 and continued for 24-96 h, A(1)AR+/+ embryos manifested growth inhibition and a disproportionate reduction in heart size, including thinner ventricular walls. Yet, when dams were exposed to hypoxia, embryos lacking A(1)ARs (A(1)AR-/-) had much more severe growth retardation than A(1)AR+/+ or +/- embryos. When levels of hypoxia-inducible factor 1alpha (HIF1alpha) were examined, A(1)AR-/- embryos had less stabilized HIF1alpha protein than A(1)AR+/- littermates. Normal patterns of cardiac gene expression were also disturbed in A(1)AR-/- embryos exposed to hypoxia. These results show that short periods of hypoxia during early embryogenesis can result in intrauterine growth retardation. We identify adenosine and A(1)ARs as playing an essential role in protecting the embryo from hypoxia.
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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.