ArticleFree radical biology & medicine2016
Superoxide dismutase 2 overexpression alleviates maternal diabetes-induced neural tube defects, restores mitochondrial function and suppresses cellular stress in diabetic embryopathy.
Article in Free radical biology & medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Lipid Remodeling in Mouse SR-B1-Deficient Embryos with Oxidative Stress-Associated Neural Tube Defects.Antioxidants (Basel, Switzerland) · 2026Article
- Exploring Research Trends and Mechanisms: Maternal Diabetes and Neural Tube Defects (1991-2023).Journal of multidisciplinary healthcare · 2025Article
- ER stress and lipid imbalance drive diabetic embryonic cardiomyopathy in an organoid model of human heart development.Stem cell reports · 2024Article
- Cell metabolism pathways involved in the pathophysiological changes of diabetic peripheral neuropathy.Neural regeneration research · 2024Review
- ER stress and lipid imbalance drive embryonic cardiomyopathy in a human heart organoid model of pregestational diabetes.bioRxiv : the preprint server for biology · 2023Article
- 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
- Angiotensin-(1-7) ameliorates high glucose-induced vascular endothelial injury through suppressing chloride channel 3.Bioengineered · 2022Article
- Circular RNA circPHKA2 Relieves OGD-Induced Human Brain Microvascular Endothelial Cell Injuries through Competitively Binding miR-574-5p to Modulate SOD2.Oxidative medicine and cellular longevity · 2021Article
- An update on the use of inositols in preventing gestational diabetes mellitus (GDM) and neural tube defects (NTDs).Expert opinion on drug metabolism & toxicology · 2020Review
- Histomorphological, VEGF and TGF-β immunoexpression changes in the diabetic rats' ovary and the potential amelioration following treatment with metformin and insulin.Journal of molecular histology · 2020Article
- Histone Post-Translational Modifications and CircRNAs in Mouse and Human Spermatozoa: Potential Epigenetic Marks to Assess Human Sperm Quality.Journal of clinical medicine · 2020Review
- The Reciprocal Causation of the ASK1-JNK1/2 Pathway and Endoplasmic Reticulum Stress in Diabetes-Induced Cognitive Decline.Frontiers in cell and developmental biology · 2020Article
- Tip60- and sirtuin 2-regulated MARCKS acetylation and phosphorylation are required for diabetic embryopathy.Nature communications · 2019Article
- High Glucose Inhibits Neural Stem Cell Differentiation Through Oxidative Stress and Endoplasmic Reticulum Stress.Stem cells and development · 2018Article
- Oxidative stress-induced miR-27a targets the redox gene nuclear factor erythroid 2-related factor 2 in diabetic embryopathy.American journal of obstetrics and gynecology · 2018Article
- The current status and future of cardiac stem/progenitor cell therapy for congenital heart defects from diabetic pregnancy.Pediatric research · 2018Review
- Endoplasmic Reticulum Stress-Induced CHOP Inhibits PGC-1α and Causes Mitochondrial Dysfunction in Diabetic Embryopathy.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Protein kinase C-alpha suppresses autophagy and induces neural tube defects via miR-129-2 in diabetic pregnancy.Nature communications · 2017Article
- Activated ClC-2 Inhibits p-Akt to Repress Myelination in GDM Newborn Rats.International journal of biological sciences · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Pregestational diabetes disrupts neurulation leading to neural tube defects (NTDs). Oxidative stress resulting from reactive oxygen species (ROS) plays a central role in the induction of NTD formation in diabetic pregnancies. We aimed to determine whether mitochondrial dysfunction increases ROS production leading to oxidative stress and diabetic embryopathy. Overexpression of the mitochondrion-specific antioxidant enzyme superoxide dismutase 2 (SOD2) in a transgenic (Tg) mouse model significantly reduced maternal diabetes-induced NTDs. SOD2 overexpression abrogated maternal diabetes-induced mitochondrial dysfunction by inhibiting mitochondrial translocation of the pro-apoptotic Bcl-2 family members, reducing the number of defective mitochondria in neuroepithelial cells, and decreasing mitochondrial membrane potential. Furthermore, SOD2 overexpression blocked maternal diabetes-increased ROS production by diminishing dihydroethidium staining signals in the developing neuroepithelium, and reducing the levels of nitrotyrosine-modified proteins and lipid hydroperoxide level in neurulation stage embryos. SOD2 overexpression also abolished maternal diabetes-induced endoplasmic reticulum stress. Finally, caspase-dependent neuroepithelial cell apoptosis enhanced by oxidative stress was significantly reduced by SOD2 overexpression. Thus, our findings support the hypothesis that mitochondrial dysfunction in the developing neuroepithelium enhances ROS production, which leads to oxidative stress and endoplasmic reticulum (ER) stress. SOD2 overexpression blocks maternal diabetes-induced oxidative stress and ER stress, and reduces the incidence of NTDs in embryos exposed to maternal diabetes.
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