Impact of maternal hyperglycemia on cardiac development: Insights from animal models.

Impact of maternal hyperglycemia on cardiac development: Insights from animal models.
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DOI:
10.1002/dvg.23449
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发表时间:
2021-11
期刊:
Genesis (New York, N.Y. : 2000)
影响因子:
--
通讯作者:
Garg V
Garg V
中科院分区:
其他
文献类型:
--
作者:
Choudhury TZ;Majumdar U;Basu M;Garg V

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先天性心脏病(CHD)是婴儿出生缺陷相关死亡的主要原因,也是全球儿科健康问题。虽然随着基因组测序技术的进步,人们越来越认识到冠心病的遗传原因,但大多数冠心病病例的病因尚不清楚。胚胎发生过程中的母体环境对心脏发育有着深远的影响,许多环境因素与冠心病风险升高有关。母亲糖尿病 (matDM) 会使婴儿患先心病的风险增加五倍。糖尿病患病率的上升导致人们越来越关注使用实验性糖尿病模型来阐明与冠心病相关的风险机制。本综述的目的是提供啮齿动物模型的全面总结,这些模型用于研究暴露于孕产妇糖尿病环境时心脏发育途径的变化,并总结这些模型的主要发现。该领域的大多数研究都利用了 matDM 的化学诱导模型,但最近也利用基于饮食和遗传的模型取得了进展。每个模型都提供了研究 matDM 独特方面的机会,对于全面了解 matDM 相关 CHD 的分子和细胞机制非常有价值。
Congenital heart disease (CHD) is the leading cause of birth-defect related death in infants and is a global pediatric health concern. While the genetic causes of CHD have become increasingly recognized with advances in genome sequencing technologies, the etiology for the majority of cases of CHD are unknown. The maternal environment during embryogenesis has a profound impact on cardiac development, and numerous environmental factors are associated with an elevated risk of CHD. Maternal diabetes (matDM) is associated with up to a five-fold increased risk of having an infant with CHD. The rising prevalence of diabetes mellitus has led to a growing interest in the use of experimental diabetic models to elucidate mechanisms underlying this associated risk for CHD. The purpose of this review is to provide a comprehensive summary of rodent models that are being used to investigate alterations in cardiac developmental pathways when exposed to a maternal diabetic setting and to summarize the key findings from these models. The majority of studies in the field have utilized the chemically induced model of matDM, but recent advances have also been made using diet-based and genetic models. Each model provides an opportunity to investigate unique aspects of matDM and are invaluable for a comprehensive understanding of the molecular and cellular mechanisms underlying matDM-associated CHD.
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