ArticleDiabetes2013
Hyperglycemia slows embryonic growth and suppresses cell cycle via cyclin D1 and p21.
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 58 citations in OpenAlex.
- Formononetin inhibits p53 signaling pathway activation to delay cellular senescence and ameliorates diabetic kidney disease.World journal of diabetes · 2026Article
- Developmental and Evolutionary Heart Adaptations Through Structure-Function Relationships.Journal of cardiovascular development and disease · 2025Review
- Zebrafish Congenital Heart Disease Models: Opportunities and Challenges.International journal of molecular sciences · 2024Review
- Osmolar Modulation Drives Reversible Cell Cycle Exit and Human Pluripotent Cell Differentiation via NF-κВ and WNT Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Maternal Pre-Existing Diabetes: A Non-Inherited Risk Factor for Congenital Cardiopathies.International journal of molecular sciences · 2023Review
- Research Progress of Maternal Metabolism on Cardiac Development and Function in Offspring.Nutrients · 2023Review
- Embryonic diapause due to high glucose is related to changes in glycolysis and oxidative phosphorylation, as well as abnormalities in the TCA cycle and amino acid metabolism.Frontiers in endocrinology · 2023Article
- Embryonic hyperglycemia perturbs the development of specific retinal cell types, including photoreceptors.Journal of cell science · 2022Article
- Article
- Embryonic nutritional hyperglycemia decreases cell proliferation in the zebrafish retina.Histochemistry and cell biology · 2022Article
- Single-cell transcriptomic profiling unveils dysregulation of cardiac progenitor cells and cardiomyocytes in a mouse model of maternal hyperglycemia.Communications biology · 2022Article
- Weighted gene co-expression identification of CDKN1A as a hub inflammation gene following cardiopulmonary bypass in children with congenital heart disease.Frontiers in surgery · 2022Article
- Hyperglycemia Altered DNA Methylation Status and Impaired Pancreatic Differentiation from Embryonic Stem Cells.International journal of molecular sciences · 2021Article
- GLUT4 in Mouse Endometrial Epithelium: Roles in Embryonic Development and Implantation.Frontiers in physiology · 2021Article
- Follow Me! A Tale of Avian Heart Development with Comparisons to Mammal Heart Development.Journal of cardiovascular development and disease · 2020Review
- Maternal Obesity Alters Placental Cell Cycle Regulators in the First Trimester of Human Pregnancy: New Insights for BRCA1.International journal of molecular sciences · 2020Article
- Bioinformatic identification and expression analysis of the chicken B cell lymphoma (BCL) gene.Genes & genomics · 2019Article
- Review
- Hyperglycemia Alters the Structure and Hemodynamics of the Developing Embryonic Heart.Journal of cardiovascular development and disease · 2018Article
- Ultrasonographic Characterization of theJournal of diabetes research · 2018Article
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5 authors at 1 institution in 1 country.
Funding
Abstract
In pregnant women, the diabetic condition results in a three- to fivefold increased risk for fetal cardiac malformations as a result of elevated glucose concentrations and the resultant osmotic stress in the developing embryo and fetus. Heart development before septation in the chick embryo was studied under two hyperglycemic conditions. Pulsed hyperglycemia induced by daily administration of glucose during 3 days of development caused daily spikes in plasma glucose concentration. In a second model, sustained hyperglycemia was induced with a single injection of glucose into the yolk on day 0. The sustained model raised the average plasma glucose concentration from 70 mg/dL to 180 mg/dL and led to decreased gene expression of glucose transporter GLUT1. Both models of hyperglycemia reduced embryo size, increased mortality, and delayed development. Within the heart outflow tract, reduced proliferation of myocardial and endocardial cells resulted from the sustained hyperglycemia and hyperosmolarity. The cell cycle inhibitor p21 was significantly increased, whereas cyclin D1, a cell cycle promoter, decreased in sustained hyperglycemia compared with controls. The evidence suggests that hyperglycemia-induced developmental delays are associated with slowed cell cycle progression, leading to reduced cellular proliferation. The suppression of critical developmental steps may underlie the cardiac defects observed during late gestation under hyperglycemic conditions.
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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.