ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2008
Early fetal hypoxia leads to growth restriction and myocardial thinning.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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Who cites it
99 citing papers in PubMed, 189 citations in OpenAlex.
- Understanding physiological adaptations of pregnancy to the chronic hypoxia of high altitude to inform obstetrical and neonatal care.Physiological reviews · 2026Review
- Insights from animal models: Dissecting the independent roles of oxygen and nutrients in the fetal origins of cardiovascular disease.The Journal of physiology · 2026Review
- Prenatal Melatonin Modulates Cardiovascular Function and Oxidative Stress in Guinea Pig Neonates Under Normoxic and Hypoxic Gestation.Antioxidants (Basel, Switzerland) · 2026Article
- Mouse placentae generated by in vitro fertilization exhibit altered gene expression, activated hypoxia responses, and reduced fitness†.Biology of reproduction · 2026Article
- Revealing the complexity of the epicardial secretome.Scientific reports · 2025Article
- Hypoxia and Multilineage Communication in 3D Organoids for Human Disease Modeling.Biomimetics (Basel, Switzerland) · 2025Review
- Comprehensive transcriptome analysis reveals MSTRG.19853.1/ssc-miR-361-3p/NPPA axis is related to hypoxic adaptation in Tibetan pigs.BMC genomics · 2025Article
- Molecular and Biochemical Mechanisms of Cardiomyopathy Development Following Prenatal Hypoxia-Focus on the NO System.Antioxidants (Basel, Switzerland) · 2025Review
- Essential roles of DCAF7/WDR68 in mouse embryonic development.Journal of translational medicine · 2025Article
- Cold-induced fibrosis and metabolic remodeling in the turtle (Trachemys scripta) ventricle.Acta physiologica (Oxford, England) · 2025Article
- Placenta-derived factors contribute to human iPSC-liver organoid growth.Nature communications · 2025Article
- Biomechanical and histomorphometric characterization of the melatonin treatment effect in the carotid artery subjected to hypobaric hypoxia.Frontiers in bioengineering and biotechnology · 2025Article
- The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024Review
- In vitro effect of vitaminBToxicology research · 2024Article
- The brain of fetuses with congenital diaphragmatic hernia shows signs of hypoxic injury with loss of progenitor cells, neurons, and oligodendrocytes.Scientific reports · 2024Article
- Integrated small RNA, mRNA and protein omics reveal a miRNA network orchestrating metabolic maturation of the developing human heart.BMC genomics · 2023Article
- Sex and age differences in social and cognitive function in offspring exposed to late gestational hypoxia.Biology of sex differences · 2023Article
- Beyond energy and growth: the role of metabolism in developmental signaling, cell behavior and diapause.Development (Cambridge, England) · 2023Article
- Sex-specific effects ofJournal of molecular and cellular cardiology plus · 2023Article
- The association between BMI trajectories and bronchopulmonary dysplasia among very preterm infants.Pediatric research · 2023Article
39 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Hypoxia is necessary for fetal development; however, excess hypoxia is detrimental. Hypoxia has been extensively studied in the near-term fetus, but less is known about earlier fetal effects. The purpose of this study was to determine the window of vulnerability to severe hypoxia, what organ system(s) is most sensitive, and why hypoxic fetuses die. We induced hypoxia by reducing maternal-inspired O2 from 21% to 8%, which decreased fetal tissue oxygenation assessed by pimonidazole binding. The mouse fetus was most vulnerable in midgestation: 24 h of hypoxia killed 89% of embryonic day 13.5 (E13.5) fetuses, but only 5% of E11.5 and 51% of E17.5 fetuses. Sublethal hypoxia at E12.5 caused growth restriction, reducing fetal weight by 26% and protein by 45%. Hypoxia induced HIF-1 target genes, including vascular endothelial growth factor (Vegf), erythropoietin, glucose transporter-1 and insulin-like growth factor binding protein-1 (Igfbp-1), which has been implicated in human intrauterine growth restriction (IUGR). Hypoxia severely compromised the cardiovascular system. Signs of heart failure, including loss of yolk sac circulation, hemorrhage, and edema, were caused by 18-24 h of hypoxia. Hypoxia induced ventricular dilation and myocardial hypoplasia, decreasing ventricular tissue by 50% and proliferation by 21% in vivo and by 40% in isolated cultured hearts. Epicardial detachment was the first sign of hypoxic damage in the heart, although expression of epicardially derived mitogens, such as FGF2, FGF9, and Wnt9b was not reduced. We propose that hypoxia compromises the fetus through myocardial hypoplasia and reduced heart rate.
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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.