ArticleCardiovascular research2011
Foetal hypoxia increases cardiac AT(2)R expression and subsequent vulnerability to adult ischaemic injury.
Article in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 71 citations in OpenAlex.
- Insights from animal models: Dissecting the independent roles of oxygen and nutrients in the fetal origins of cardiovascular disease.The Journal of physiology · 2026Review
- Structural and Functional Abnormalities in the Preterm Heart: From Development to Adulthood.Journal of the American Heart Association · 2026Review
- Effects of Sex Hormones on Vascular Reactivity in Boys With Hypospadias.The Journal of clinical endocrinology and metabolism · 2024Article
- The impact of COVID-19 on populations living at high altitude: Role of hypoxia-inducible factors (HIFs) signaling pathway in SARS-CoV-2 infection and replication.Frontiers in physiology · 2022Article
- Programming With Varying Dietary Fat Content Alters Cardiac Insulin Receptor, Glut4 and FoxO1 Immunoreactivity in Neonatal Rats, Whereas High Fat Programming Alters Cebpa Gene Expression in Neonatal Female Rats.Frontiers in endocrinology · 2021Article
- Multi-Omics Integration Reveals Short and Long-Term Effects of Gestational Hypoxia on the Heart Development.Cells · 2019Article
- Prenatal hypoxia-induced epigenomic and transcriptomic reprogramming in rat fetal and adult offspring hearts.Scientific data · 2019Article
- Review
- Foetal hypoxia impacts methylome and transcriptome in developmental programming of heart disease.Cardiovascular research · 2019Article
- Glucocorticoids and programming of the microenvironment in heart.The Journal of endocrinology · 2019Review
- Long-term exposure to high altitude hypoxia during pregnancy increases fetal heart susceptibility to ischemia/reperfusion injury and cardiac dysfunction.International journal of cardiology · 2019Article
- Employing Macrophage-Derived Microvesicle for Kidney-Targeted Delivery of Dexamethasone: An Efficient Therapeutic Strategy against Renal Inflammation and Fibrosis.Theranostics · 2019Article
- High Fat Programming and Cardiovascular Disease.Medicina (Kaunas, Lithuania) · 2018Review
- The detrimental effects of glucocorticoids exposure during pregnancy on offspring's cardiac functions mediated by hypermethylation of bone morphogenetic protein-4.Cell death & disease · 2018Article
- Recombinant relaxin protects liver transplants from ischemia damage by hepatocyte glucocorticoid receptor: From bench-to-bedside.Hepatology (Baltimore, Md.) · 2018Article
- Gestational Hypoxia and Developmental Plasticity.Physiological reviews · 2018Review
- SIRT1 increases cardiomyocyte binucleation in the heart development.Oncotarget · 2018Article
- MicroRNA-210 suppresses glucocorticoid receptor expression in response to hypoxia in fetal rat cardiomyocytes.Oncotarget · 2017Article
- Ischemia/Reperfusion.Comprehensive Physiology · 2016Review
- An Intronic Enhancer Element Regulates Angiotensin II Type 2 Receptor Expression during Satellite Cell Differentiation, and Its Activity Is Suppressed in Congestive Heart Failure.The Journal of biological chemistry · 2016Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
aimsHypoxia is a common stress to the foetus and results in increased cardiac vulnerability to adult ischaemic injury. This study tested the hypothesis that foetal hypoxia causes programming of increased AT(2) receptor (AT(2)R) expression in the heart, resulting in the heightened cardiac susceptibility to adult ischaemic injury. METHODS AND
resultsTime-dated pregnant rats were divided between normoxic and hypoxic (10.5% O(2) from days 15 to 21 of gestation) groups. Hypoxia resulted in significantly increased AT(2)R in the heart of adult offspring. Multiple glucocorticoid response elements (GREs) were identified at the AT(2)R promoter, deletion of which increased the promoter activity. Consistently, ex vivo treatment of isolated foetal hearts with dexamethasone for 48 h decreased AT(2)R expression, which was inhibited by RU 486. Hypoxia decreased glucocorticoid receptors (GRs) in the hearts of foetal, 3-week-old and 3-month-old offspring, resulting in decreased GR binding to the GREs at the AT(2)R promoter. The inhibition of AT(2)R improved postischaemic recovery of left ventricular function and rescued the foetal hypoxia-induced cardiac ischaemic vulnerability in male adult animals. In contrast, the inhibition of AT(1) receptors decreased the postischaemic recovery.
conclusionThe results demonstrate that in utero hypoxia causes programming of increased AT(2)R gene expression in the heart by downregulating GR, which contributes to the increased cardiac vulnerability to adult ischaemic injury caused by prenatal hypoxic exposure.
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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.