ArticleMolecular and cellular biochemistry2014
Gestational hypertension and the developmental origins of cardiac hypertrophy and diastolic dysfunction.
Article in Molecular and cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Multi-Organ Phenotypes of Offspring Born Following Hypertensive Disorders of Pregnancy: A Systematic Review.Journal of the American Heart Association · 2024Pooled it
- Axl deficiency promotes preeclampsia and vascular malformations in mice.Molecular therapy. Nucleic acids · 2025Article
- The Influence of Maternal Condition on Fetal Cardiac Function during the Second Trimester.Diagnostics (Basel, Switzerland) · 2023Article
- Natriuretic Peptide Signaling in Uterine Biology and Preeclampsia.International journal of molecular sciences · 2023Review
- Chronic Hypertension in Pregnancy: A Lens Into Cardiovascular Disease Risk and Prevention.Hypertension (Dallas, Tex. : 1979) · 2023Review
- What Is the Impact of Maternal Hypertension on Offspring Cardiac Structure and Function?JACC. Advances · 2022Article
- Assessment of myocardial injury in neonates born to pregnant women with pregnancy complicated by severe preeclampsia by myocardial work indices: a prospective study.Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2022Article
- Krüppel-like factor 17 upregulates uterine corin expression and promotes spiral artery remodeling in pregnancy.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Prenatal and Postnatal Cardiac Development in Offspring of Hypertensive Pregnancies.Journal of the American Heart Association · 2020Article
- Developmental origins of pregnancy-induced cardiac changes: establishment of a novel model using the atrial natriuretic peptide gene-disrupted mice.Molecular and cellular biochemistry · 2018Article
- Cardiometabolic Health Among Adult Offspring of Hypertensive Pregnancies: The Cardiovascular Risk in Young Finns Study.Journal of the American Heart Association · 2018Article
- Maternal hypertension programs increased cerebral tissue damage following stroke in adult offspring.Molecular and cellular biochemistry · 2015Article
- Placental growth factor influences maternal cardiovascular adaptation to pregnancy in mice.Biology of reproduction · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The developmental origins of health and disease refer to the theory that adverse maternal environments influence fetal development and the risk of cardiovascular disease in adulthood. We used the chronically hypertensive atrial natriuretic peptide knockout (ANP-/-) mouse as a model of gestational hypertension, and attempted to determine the effect of gestational hypertension on left ventricular (LV) structure and function in adult offspring. We crossed normotensive ANP+/+ females with ANP-/- males (yielding ANP+/-(WT) offspring) and hypertensive ANP-/- females with ANP+/+ males (yielding ANP+/-(KO) offspring). Cardiac gene expression was measured using real-time quantitative PCR. Cardiac function was assessed using echocardiography. Daily injections of isoproterenol (ISO) were used to induce cardiac stress. Collagen deposition was assessed using picrosirius red staining. All mice were 10 weeks of age. Gestational hypertension resulted in significant LV hypertrophy in offspring, with no change in LV function. Treatment with ISO resulted in significant LV diastolic dysfunction with a restrictive filling pattern (increased E/A ratio and E/e') and interstitial myocardial fibrosis only in ANP+/-(KO) and not ANP+/-(WT) offspring. Gestational hypertension programs adverse LV structural and functional remodeling in offspring. These data suggest that adverse maternal environments may increase the risk of heart failure in offspring later in life.
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