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Heart Disease Link to Fetal Hypoxia and Oxidative Stress
Open accessAbstract
The quality of the intrauterine environment interacts with our genetic makeup to shape the risk of developing disease in later life. Fetal chronic hypoxia is a common complication of pregnancy. This chapter reviews how fetal chronic hypoxia programmes cardiac and endothelial dysfunction in the offspring in adult life and discusses the mechanisms via which this may occur. Using an integrative approach in large and small animal models at the in vivo, isolated organ, cellular and molecular levels, our programmes of work have raised the hypothesis that oxidative stress in the fetal heart and vasculature underlies the mechanism via which prenatal hypoxia programmes cardiovascular dysfunction in later life. Developmental hypoxia independent of changes in maternal nutrition promotes fetal growth restriction and induces changes in the cardiovascular, metabolic and endocrine systems of the adult offspring, which are normally associated with disease states during ageing. Treatment with antioxidants of animal pregnancies complicated with reduced oxygen delivery to the fetus prevents the alterations in fetal growth, and the cardiovascular, metabolic and endocrine dysfunction in the fetal and adult offspring. The work reviewed offers both insight into mechanisms and possible therapeutic targets for clinical intervention against the early origin of cardiometabolic disease in pregnancy complicated by fetal chronic hypoxia.
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The links between impaired placental function and fetal outcomes go beyond abnormal maternal nutrient supply and include intrauterine hypoxia, maternal social stress leading to hypercortisolemia, and environmental toxins.
“These links go beyond an abnormal maternal nutrient supply, and include, for example, intrauterine hypoxia (213), maternal social stress of the severity that leads to hypercortisolemia (128) and, increasingly, environmental toxins.”
From Placental Origins of Chronic Disease (2016) · cites this paper as [213]
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Metadata
- Authors
- Giussani, D. A., Niu, Y., Herrera, E. A., Richter, H. G., Camm, E. J., Thakor, A. S., Kane, A. D., Hansell, J. A., Brain, K. L., Skeffington, K. L., Itani, N., Wooding, F. B. P., Cross, C. M., & Allison, B. J.
- Affiliations
- University of Cambridge (GB)
- University of Chile (CL)
- Austral University of Chile (CL)
- Corresponding author
- Giussani, Dino A.
- ORCID
- Venue
- Advances in Experimental Medicine and Biology
- Publisher
- Springer New York
- Published
- 2014
- Volume
- 814
- Pages
- 77-87
- ISSN
- 0065-2598 (ISSN-L)
- 2214-8019
- OpenAlex
- W135451564
- Cited by
- 81
- References
- 85
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 5 · 2023: 10 · 2022: 9 · 2021: 6 · 2020: 6 · 2019: 7 · 2018: 5 · 2017: 7 · 2016: 9 · 2015: 10 · 2014: 1
- FWCI
- 69.00
- Type
- book chapter
- Language
- en
- Open access
- Licence
- Locations
- Advances in experimental medicine and biology (publishedVersion)
- PubMed (publishedVersion)
- Universidad de Chile (submittedVersion, cc-by-nc-nd)
- Funders
- British Heart Foundation (PG/10/99/28656, RG/11/16/29260, PG/14/5/30547, FS/12/74/29778)
- Biotechnology and Biological Sciences Research Council (BB/E002668/1)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Keywords
- fetal hypoxia, oxidative stress, heart disease, developmental programming, fetal growth restriction, cardiovascular dysfunction, endothelial dysfunction, cardiometabolic disease, antioxidants, pregnancy complications, aging
- MeSH terms
- Female, Fetal Hypoxia, Heart Diseases, Humans, Pregnancy, Prenatal Exposure Delayed Effects, Oxidative Stress
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