ReviewAntioxidants (Basel, Switzerland)2019
Say NO to ROS: Their Roles in Embryonic Heart Development and Pathogenesis of Congenital Heart Defects in Maternal Diabetes.
Review in Antioxidants (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- The Role of Selenium During Gestation in the Development of Fetal Congenital Anomalies: A Systematic Review.Nutrients · 2026Pooled it
- Hypoplastic Left Heart Syndrome Cardiomyocytes Exhibit Intrinsic Stress Vulnerabilities and Augmented Stress Responses in vitro.Stem cell reviews and reports · 2026Article
- Prenatal Melatonin Modulates Cardiovascular Function and Oxidative Stress in Guinea Pig Neonates Under Normoxic and Hypoxic Gestation.Antioxidants (Basel, Switzerland) · 2026Article
- Haploinsufficiency of Endothelial Nitric Oxide Synthase Mitigates Beneficial Effects of Maternal Exercise on Fetal Heart Development During Pregestational Diabetes.Journal of the American Heart Association · 2026Article
- Relationship between maternal iron status and the risk of congenital heart defects: A case-control study.The Journal of international medical research · 2025Article
- Calorie restriction mimetics against aging and inflammation.Biogerontology · 2025Review
- Predictive Value of Maternal HbA1c Levels for Fetal Hypertrophic Cardiomyopathy in Pregestational Diabetic Pregnancies.Children (Basel, Switzerland) · 2025Article
- Enhancing antioxidant activity of rice protein hydrolysates through glycosylation modification.Frontiers in nutrition · 2025Article
- Investigation of the mechanism of hypertension caused by BTKi in the treatment of hematologic diseases.Frontiers in pharmacology · 2025Review
- An Overview of Adverse Outcome Pathway Links between PMEnvironment & health (Washington, D.C.) · 2024Review
- The NOS/NO System in Renal Programming and Reprogramming.Antioxidants (Basel, Switzerland) · 2023Review
- ER stress and lipid imbalance drive embryonic cardiomyopathy in a human heart organoid model of pregestational diabetes.bioRxiv : the preprint server for biology · 2023Article
- Effect of maternal pregestational diabetes mellitus on congenital heart diseases.World journal of pediatrics : WJP · 2023Review
- Maternal nicotine exposure induces congenital heart defects in the offspring of mice.Journal of cellular and molecular medicine · 2022Article
- Exerkine apelin reverses obesity-associated placental dysfunction by accelerating mitochondrial biogenesis in mice.American journal of physiology. Endocrinology and metabolism · 2022Article
- Review
- Role of PI3K/Akt signaling pathway in cardiac fibrosis.Molecular and cellular biochemistry · 2021Review
- Review
- The role of glucose in physiological and pathological heart formation.Developmental biology · 2021Review
- Association and interaction effect of UCP2 gene polymorphisms and dietary factors with congenital heart diseases in Chinese Han population.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Congenital heart defects (CHDs) are the most prevalent and serious birth defect, occurring in 1% of all live births. Pregestational maternal diabetes is a known risk factor for the development of CHDs, elevating the risk in the child by more than four-fold. As the prevalence of diabetes rapidly rises among women of childbearing age, there is a need to investigate the mechanisms and potential preventative strategies for these defects. In experimental animal models of pregestational diabetes induced-CHDs, upwards of 50% of offspring display congenital malformations of the heart, including septal, valvular, and outflow tract defects. Specifically, the imbalance of nitric oxide (NO) and reactive oxygen species (ROS) signaling is a major driver of the development of CHDs in offspring of mice with pregestational diabetes. NO from endothelial nitric oxide synthase (eNOS) is crucial to cardiogenesis, regulating various cellular and molecular processes. In fact, deficiency in eNOS results in CHDs and coronary artery malformation. Embryonic hearts from diabetic dams exhibit eNOS uncoupling and oxidative stress. Maternal treatment with sapropterin, a cofactor of eNOS, and antioxidants such as N-acetylcysteine, vitamin E, and glutathione as well as maternal exercise have been shown to improve eNOS function, reduce oxidative stress, and lower the incidence CHDs in the offspring of mice with pregestational diabetes. This review summarizes recent data on pregestational diabetes-induced CHDs, and offers insights into the important roles of NO and ROS in embryonic heart development and pathogenesis of CHDs in maternal diabetes.
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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.