ArticleAmerican journal of obstetrics and gynecology2017
Pregestational type 2 diabetes mellitus induces cardiac hypertrophy in the murine embryo through cardiac remodeling and fibrosis.
Article in American journal of obstetrics and gynecology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- Maternal hyperglycemia-induced O-GlcNAcylation of CaMKIIδ promotes mtDNA release and cardiac remodeling in offspring.Nature communications · 2026Article
- Reversal of canonical Wnt/β-catenin signaling pathway attenuates gestational diabetes mellitus-induced offspring cardiac hypertrophy: mechanistic insights into pathological remodeling.Nutrition & diabetes · 2026Article
- The Progression of Cardiac Damage in the Offspring of Mothers with Gestational Diabetes Is Regulated by the p53/miR-34/SIRT1/7 Pathway.International journal of molecular sciences · 2026Article
- The mechanism of maternal inheritance of glycolipid metabolism disorder in a zebrafish model of type 2 diabetes.Scientific reports · 2025Article
- Predictive Value of Maternal HbA1c Levels for Fetal Hypertrophic Cardiomyopathy in Pregestational Diabetic Pregnancies.Children (Basel, Switzerland) · 2025Article
- Small Molecule Activators of Mitochondrial Fusion Prevent Congenital Heart Defects Induced by Maternal Diabetes.JACC. Basic to translational science · 2024Article
- Changes in the shape and function of the fetal heart of pre- and gestational diabetes mothers.BMC pregnancy and childbirth · 2024Article
- Quantifying fetal heart health in gestational diabetes: a new approach with fetal heart quantification technology.Frontiers in pharmacology · 2024Article
- Programming of cardiometabolic health: the role of maternal and fetal hyperinsulinaemia.The Journal of endocrinology · 2022Review
- Inhibition of SGLT1 Alleviates the Glycemic Variability-Induced Cardiac Fibrosis via Inhibition of Activation of Macrophage and Cardiac Fibroblasts.Molecular and cellular biology · 2022Article
- Protective Roles of Apigenin Against Cardiometabolic Diseases: A Systematic Review.Frontiers in nutrition · 2022Review
- Insulin-Induced Cardiomyocytes Hypertrophy That Is Prevented by Taurine via β-alanine-Sensitive NaNutrients · 2021Article
- Deficiency of the oxidative stress-responsive kinase p70S6K1 restores autophagy and ameliorates neural tube defects in diabetic embryopathy.American journal of obstetrics and gynecology · 2020Article
- Cardiac Function in Infants Born to Mothers With Gestational Diabetes - Estimation of Early Diastolic Intraventricular Pressure Differences.Circulation reports · 2019Article
- The increased activity of a transcription factor inhibits autophagy in diabetic embryopathy.American journal of obstetrics and gynecology · 2019Article
- LncRNAs and miRs as epigenetic signatures in diabetic cardiac fibrosis: new advances and perspectives.Endocrine · 2018Review
- The current status and future of cardiac stem/progenitor cell therapy for congenital heart defects from diabetic pregnancy.Pediatric research · 2018Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCardiac hypertrophy is highly prevalent in patients with type 2 diabetes mellitus. Experimental evidence has implied that pregnant women with type 2 diabetes mellitus and their children are at an increased risk of cardiovascular diseases. Our previous mouse model study revealed that maternal type 2 diabetes mellitus induces structural heart defects in their offspring.
objectiveThis study aims to determine whether maternal type 2 diabetes mellitus induces embryonic heart hypertrophy in a murine model of diabetic embryopathy. STUDY
designThe type 2 diabetes mellitus embryopathy model was established by feeding 4-week-old female C57BL/6J mice with a high-fat diet for 15 weeks. Cardiac hypertrophy in embryos at embryonic day 17.5 was characterized by measuring heart size and thickness of the right and left ventricle walls and the interventricular septum, as well as the expression of β-myosin heavy chain, atrial natriuretic peptide, insulin-like growth factor-1, desmin, and adrenomedullin. Cardiac remodeling was determined by collagen synthesis and fibronectin synthesis. Fibrosis was evaluated by Masson staining and determining the expression of connective tissue growth factor, osteopontin, and galectin-3 genes. Cell apoptosis also was measured in the developing heart.
resultsThe thicknesses of the left ventricle walls and the interventricular septum of embryonic hearts exposed to maternal diabetes were significantly thicker than those in the nondiabetic group. Maternal diabetes significantly increased β-myosin heavy chain, atrial natriuretic peptide, insulin-like growth factor-1, and desmin expression, but decreased expression of adrenomedullin. Moreover, collagen synthesis was significantly elevated, whereas fibronectin synthesis was suppressed, in embryonic hearts from diabetic dams, suggesting that cardiac remodeling is a contributing factor to cardiac hypertrophy. The cardiac fibrosis marker, galectin-3, was induced by maternal diabetes. Furthermore, maternal type 2 diabetes mellitus activated the proapoptotic c-Jun-N-terminal kinase 1/2 stress signaling and triggered cell apoptosis by increasing the number of terminal deoxynucleotidyl transferase 2'-deoxyuridine 5'-triphosphate nick end labeling-positive cells (10.4 ± 2.2% of the type 2 diabetes mellitus group vs 3.8 ± 0.7% of the nondiabetic group, P < .05).
conclusionMaternal type 2 diabetes mellitus induces cardiac hypertrophy in embryonic hearts. Adverse cardiac remodeling, including elevated collagen synthesis, suppressed fibronectin synthesis, profibrosis, and apoptosis, is implicated as the etiology of cardiac hypertrophy.
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