ArticleDiabetes2008
Decreased cardiac glutathione peroxidase levels and enhanced mandibular apoptosis in malformed embryos of diabetic rats.
Article in Diabetes, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 63 citations in OpenAlex.
- Exploring Endoplasmic Reticulum Stress in Gestational Diabetes Mellitus: MultiOmics Insights Through Mendelian Randomization.International journal of women's health · 2026Article
- Role of Maternal Obesity in Offspring Cardiovascular Development and Congenital Heart Defects.Journal of the American Heart Association · 2025Article
- Guidelines for in vivo models of developmental programming of cardiovascular disease risk.American journal of physiology. Heart and circulatory physiology · 2024Review
- Maternal Pre-Existing Diabetes: A Non-Inherited Risk Factor for Congenital Cardiopathies.International journal of molecular sciences · 2023Review
- Functional cargos of exosomes derived from Flk-1Communications biology · 2022Article
- Impact of maternal hyperglycemia on cardiac development: Insights from animal models.Genesis (New York, N.Y. : 2000) · 2021Review
- Mending a broken heart:Disease models & mechanisms · 2021Review
- Defensive impact of propolis against CClJournal of advanced veterinary and animal research · 2021Article
- Progress in the emerging role of selenoproteins in cardiovascular disease: focus on endoplasmic reticulum-resident selenoproteins.Cellular and molecular life sciences : CMLS · 2019Review
- Maternal hyperglycemia and fetal cardiac development: Clinical impact and underlying mechanisms.Birth defects research · 2018Review
- Pregestational type 2 diabetes mellitus induces cardiac hypertrophy in the murine embryo through cardiac remodeling and fibrosis.American journal of obstetrics and gynecology · 2017Article
- Embryonic defence mechanisms against glucose-dependent oxidative stress require enhanced expression of Alx3 to prevent malformations during diabetic pregnancy.Scientific reports · 2017Article
- Type 2 diabetes mellitus induces congenital heart defects in murine embryos by increasing oxidative stress, endoplasmic reticulum stress, and apoptosis.American journal of obstetrics and gynecology · 2016Article
- Reevaluation of Antioxidative Strategies for Birth Defect Prevention in Diabetic Pregnancies.Journal of biomolecular research & therapeutics · 2016Article
- The status of diabetic embryopathy.Upsala journal of medical sciences · 2016Review
- High Glucose-Repressed CITED2 Expression Through miR-200b Triggers the Unfolded Protein Response and Endoplasmic Reticulum Stress.Diabetes · 2016Article
- Dominant negative FADD dissipates the proapoptotic signalosome of the unfolded protein response in diabetic embryopathy.American journal of physiology. Endocrinology and metabolism · 2015Article
- Superoxide Dismutase 1 In Vivo Ameliorates Maternal Diabetes Mellitus-Induced Apoptosis and Heart Defects Through Restoration of Impaired Wnt Signaling.Circulation. Cardiovascular genetics · 2015Article
- ASK1 mediates the teratogenicity of diabetes in the developing heart by inducing ER stress and inhibiting critical factors essential for cardiac development.American journal of physiology. Endocrinology and metabolism · 2015Article
- Cellular Stress, Excessive Apoptosis, and the Effect of Metformin in a Mouse Model of Type 2 Diabetic Embryopathy.Diabetes · 2015Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo characterize normal and malformed embryos within the same litters from control and diabetic rats for expression of genes related to metabolism of reactive oxygen species (ROS) or glucose as well as developmental genes. RESEARCH DESIGN AND
methodsEmbryos from nondiabetic and streptozotocin-induced diabetic rats were collected on gestational day 11 and evaluated for gene expression (PCR) and distribution of activated caspase-3 and glutathione peroxidase (Gpx)-1 by immunohistochemistry.
resultsMaternal diabetes (MD group) caused growth retardation and an increased malformation rate in the embryos of MD group rats compared with those of controls (N group). We found decreased gene expression of Gpx-1 and increased expression of vascular endothelial growth factor-A (Vegf-A) in malformed embryos of diabetic rats (MDm group) compared with nonmalformed littermates (MDn group). Alterations of messenger RNA levels of other genes were similar in MDm and MDn embryos. Thus, expression of copper zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD), and sonic hedgehog homolog (Shh) were decreased, and bone morphogenetic protein-4 (Bmp-4) was increased, in the MD embryos compared with the N embryos. In MDm embryos, we detected increased activated caspase-3 immunostaining in the first visceral arch and cardiac area and decreased Gpx-1 immunostaining in the cardiac tissue; both findings differed from the caspase/Gpx-1 immunostaining of the MDn and N embryos.
conclusionsMaternal diabetes causes growth retardation, congenital malformations, and decreased general antioxidative gene expression in the embryo. In particular, enhanced apoptosis of the first visceral arch and heart, together with decreased cardiac Gpx-1 levels, may compromise the mandible and heart and thus cause an increased risk of developing congenital malformation.
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