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Advanced glycation end products induce neural tube defects through elevating oxidative stress in mice 预览
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作者 Ru-Lin Li Wei-Wei Zhao Bing-Yan Gao 《中国神经再生研究:英文版》 SCIE CAS CSCD 2018年第8期1368-1374,共7页
关键词 氧化应力 试管 神经 产品 老鼠 氧化压力 NTD H202
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Birth defects in pregestational diabetes: Defect range,glycemic threshold and pathogenesis 预览
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作者 Rinat Gabbay-Benziv E Albert Reece Fang Wang, Peixin Yang 《世界糖尿病杂志:英文版(电子版)》 SCIE 2015年第3期481-488,共8页
Currently, 60 million women of reproductive age(18-44 years old) worldwide, and approximately 3million American women have diabetes mellitus, andit has been estimated that this number will doubleby 2030. Pregestatio... Currently, 60 million women of reproductive age(18-44 years old) worldwide, and approximately 3million American women have diabetes mellitus, andit has been estimated that this number will doubleby 2030. Pregestational diabetes mellitus (PGD) is asignificant public health problem that increases therisk for structural birth defects affecting both maternaland neonatal pregnancy outcome. The most commontypes of human structural birth defects associated withPGD are congenital heart defects and central nervoussystem defects. However, diabetes can induce birthdefects in any other fetal organ. In general, the rateof birth defects increases linearly with the degree ofmaternal hyperglycemia, which is the major factor thatmediates teratogenicity of PGD. Stringent prenatal careand glycemic control are effective means to reducebirth defects in PGD pregnancies, but cannot reducethe incidence of birth defects to the rate of that is seenin the nondiabetic population. Studies in animal modelshave revealed that PGD induces oxidative stress,which activates cellular stress signalling leading todysregulation of gene expression and excess apoptosisin the target organs, including the neural tube andembryonic heart. Activation of the apoptosis signalregulatingkinase 1 (ASK1)-forkhead transcription factor3a (FoxO3a)-caspase 8 pathway causes apoptosis in thedeveloping neural tube leading to neural tube defects(NTDs). ASK1 activates the c-Jun-N-Terminal kinase1/2 (JNK1/2), which leads to activation of the unfoldedprotein response and endoplasmic reticulum (ER) stress.Deletion of the ASK1 gene, the JNK1 gene, or the JNK2gene, or inhibition of ER stress by 4-Phenylbutyric acidabrogates diabetes-induced apoptosis and reduces theformation of NTDs. Antioxidants, such as thioredoxin,which inhibits the ASK1-FoxO3a-caspase 8 pathway orER stress inhibitors, may prevent PGD-induced birthdefects. Gabbay-Benziv R et al . Birth defects in pregestational diabetes 展开更多
关键词 Pregestational diabetes BIRTH defects Glycemic THRESHOLD DIABETIC embryopathy RANGE ofdefects
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