• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

胎儿对胎盘功能不全所致慢性缺氧的适应机制:综述。

Mechanisms of Fetal Adaptation to Chronic Hypoxia following Placental Insufficiency: A Review.

机构信息

Obstetrics and Gynaecology Unit, Department of Medicine and Surgery, University of Parma, Parma, Italy.

Department of Obstetrics and Gynaecology, University Hospital rechts der Isar, Technical University of Munich, Munich, Germany.

出版信息

Fetal Diagn Ther. 2022;49(5-6):279-292. doi: 10.1159/000525717. Epub 2022 Jun 27.

DOI:10.1159/000525717
PMID:35760055
Abstract

Placental insufficiency is associated with reduced oxygen and nutrient supply to the fetus, which may result in fetal growth restriction (FGR). In an attempt to cope with the hostile intrauterine environment, FGR fetuses respond through metabolic, endocrine, vascular, cardiac, behavioral, hematological, and immunological adaptive mechanisms. However, permanent sequelae may result from such adaptive mechanisms. In this review, we describe the mechanisms of fetal adaptation to the hostile intrauterine environment in FGR of uteroplacental origin and detail their pathophysiology and potential implications for the extrauterine life of the individual.

摘要

胎盘功能不全与胎儿供氧和营养供应减少有关,这可能导致胎儿生长受限(FGR)。为了应对恶劣的宫内环境,FGR 胎儿通过代谢、内分泌、血管、心脏、行为、血液和免疫适应机制做出反应。然而,这种适应机制可能会导致永久性的后遗症。在这篇综述中,我们描述了胎儿对源自胎盘的 FGR 中恶劣的宫内环境的适应机制,并详细介绍了它们的病理生理学及其对个体宫外生活的潜在影响。

相似文献

1
Mechanisms of Fetal Adaptation to Chronic Hypoxia following Placental Insufficiency: A Review.胎儿对胎盘功能不全所致慢性缺氧的适应机制:综述。
Fetal Diagn Ther. 2022;49(5-6):279-292. doi: 10.1159/000525717. Epub 2022 Jun 27.
2
Adaptive responses in uteroplacental metabolism and fetoplacental nutrient shuttling and sensing during placental insufficiency.胎盘功能不全时,子宫胎盘代谢和胎儿胎盘营养转运及感应的适应性反应。
Am J Physiol Endocrinol Metab. 2023 Jun 1;324(6):E556-E568. doi: 10.1152/ajpendo.00046.2023. Epub 2023 Apr 26.
3
Adaptations of the human placenta to hypoxia: opportunities for interventions in fetal growth restriction.人类胎盘对缺氧的适应:干预胎儿生长受限的机会。
Hum Reprod Update. 2021 Apr 21;27(3):531-569. doi: 10.1093/humupd/dmaa053.
4
The relationship between transplacental O2 diffusion and placental expression of PlGF, VEGF and their receptors in a placental insufficiency model of fetal growth restriction.胎儿生长受限胎盘功能不全模型中经胎盘氧扩散与胎盘PlGF、VEGF及其受体表达之间的关系
J Physiol. 2003 Jul 15;550(Pt 2):641-56. doi: 10.1113/jphysiol.2003.039511. Epub 2003 May 9.
5
Cardiac function in fetal growth restriction.胎儿生长受限的心脏功能。
Minerva Obstet Gynecol. 2021 Aug;73(4):423-434. doi: 10.23736/S2724-606X.21.04787-0. Epub 2021 Apr 27.
6
Chronic hypoxia in pregnant mice impairs the placental and fetal vascular response to acute hypercapnia in BOLD-MRI hemodynamic response imaging.慢性缺氧会损害怀孕小鼠在 BOLD-MRI 血流动力学反应成像中胎盘和胎儿对急性高碳酸血症的血管反应。
Placenta. 2021 Jul;110:29-38. doi: 10.1016/j.placenta.2021.05.006. Epub 2021 Jun 3.
7
eNOS knockout mouse as a model of fetal growth restriction with an impaired uterine artery function and placental transport phenotype.eNOS 敲除小鼠作为胎儿生长受限模型,其具有子宫动脉功能障碍和胎盘转运表型。
Am J Physiol Regul Integr Comp Physiol. 2012 Jul 1;303(1):R86-93. doi: 10.1152/ajpregu.00600.2011. Epub 2012 May 2.
8
Interventions for placental insufficiency and fetal growth restriction.干预胎盘功能不全和胎儿生长受限。
Placenta. 2022 Jul;125:4-9. doi: 10.1016/j.placenta.2022.03.127. Epub 2022 Apr 4.
9
The fetal response to chronic placental insufficiency.胎儿对慢性胎盘功能不全的反应。
Semin Perinatol. 2008 Jun;32(3):201-5. doi: 10.1053/j.semperi.2007.11.002.
10
Novel use of proton magnetic resonance spectroscopy (1HMRS) to non-invasively assess placental metabolism.利用质子磁共振波谱(1HMRS)无创评估胎盘代谢。
PLoS One. 2012;7(8):e42926. doi: 10.1371/journal.pone.0042926. Epub 2012 Aug 10.

引用本文的文献

1
Smoke signals in the genome: Epigenetic consequences of parental tobacco exposure (Review).基因组中的烟雾信号:父母烟草暴露的表观遗传学后果(综述)
Biomed Rep. 2025 Jun 23;23(3):146. doi: 10.3892/br.2025.2024. eCollection 2025 Sep.
2
Changes to the Haematological Parameters of Rat Offspring Born From High Fat High Carbohydrate (HFHC) Diet-Induced Prediabetic and Preeclamptic Sprague Dawley Rats: Assessing the Effects on Selected Haematological Markers.高脂高碳水化合物(HFHC)饮食诱导的糖尿病前期和子痫前期斯普拉格-道利大鼠所产仔鼠血液学参数的变化:评估对选定血液学标志物的影响。
Diabetes Metab Syndr Obes. 2025 Mar 21;18:831-845. doi: 10.2147/DMSO.S436001. eCollection 2025.
3
The potential role of the αVβ3 integrin receptor in placental biology and normal and complicated pregnancies.
αVβ3整合素受体在胎盘生物学以及正常和复杂妊娠中的潜在作用。
Br J Haematol. 2025 Apr;206(4):1054-1061. doi: 10.1111/bjh.20019. Epub 2025 Feb 20.
4
Prenatal alcohol exposure is associated with altered feto-placental blood flow and sex-specific placental changes.产前酒精暴露与胎儿-胎盘血流改变及性别特异性胎盘变化有关。
JCI Insight. 2025 Feb 10;10(3):e186096. doi: 10.1172/jci.insight.186096.
5
Relative uteroplacental insufficiency of labor.相对产时子宫胎盘功能不全。
Acta Obstet Gynecol Scand. 2024 Oct;103(10):1910-1918. doi: 10.1111/aogs.14937. Epub 2024 Aug 6.
6
Advanced magnetic resonance imaging detects altered placental development in pregnancies affected by congenital heart disease.高级磁共振成像检测到先天性心脏病胎儿的胎盘发育改变。
Sci Rep. 2024 May 29;14(1):12357. doi: 10.1038/s41598-024-63087-8.
7
Advanced magnetic resonance imaging detects altered placental development in pregnancies affected by congenital heart disease.先进的磁共振成像技术可检测出受先天性心脏病影响的妊娠中胎盘发育的改变。
Res Sq. 2024 Jan 23:rs.3.rs-3873412. doi: 10.21203/rs.3.rs-3873412/v1.
8
Total and Regional Brain Volumes in Fetuses With Congenital Heart Disease.胎儿先天性心脏病的全脑和局部脑容量。
J Magn Reson Imaging. 2024 Aug;60(2):497-509. doi: 10.1002/jmri.29078. Epub 2023 Oct 17.
9
Incidence, clinical features and perinatal outcome in anomalous fetuses with late-onset growth restriction: cohort study.晚发型生长受限异常胎儿的发生率、临床特征及围产儿结局:队列研究。
Ultrasound Obstet Gynecol. 2022 Nov;60(5):632-639. doi: 10.1002/uog.24961.