Pathophysiology of placental-derived fetal growth restriction

Placental-related fetal growth restriction arises primarily due to deficient remodeling of the uterine spiral arteries supplying the placenta during early pregnancy. The resultant malperfusion induces cell stress within the placental tissues, leading to selective suppression of protein synthesis and...

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Published in	American journal of obstetrics and gynecology Vol. 218; no. 2; pp. S745 - S761
Main Authors	Burton, Graham J., Jauniaux, Eric
Format	Journal Article
Language	English
Published	United States Elsevier Inc 01.02.2018
Subjects	AKT/mTOR apoptosis atherosis chorion laeve Chorionic Villi - metabolism Chorionic Villi - pathology Chorionic Villi - physiopathology electron transport chain extravillous trophoblast failure of physiologic transformation Female fetal growth restriction Fetal Growth Retardation - etiology Fetal Growth Retardation - metabolism Fetal Growth Retardation - physiopathology fetoplacental weight ratio Gene Expression Regulation Genomic Imprinting hemochorial placentation Humans interstitial trophoblast intervillous space intraplacental oxygen concentration Magnetic Resonance Imaging Maternal-Fetal Exchange mitochondria oxidative stress perivillous fibrin deposition placenta Placenta - diagnostic imaging Placenta - pathology Placental Circulation placental infarct placental inflammation Placental Insufficiency - diagnostic imaging Placental Insufficiency - metabolism Placental Insufficiency - pathology Placental Insufficiency - physiopathology placental location Placentation Pre-Eclampsia - metabolism Pre-Eclampsia - physiopathology Pregnancy reactive oxygen species spiral arteries Stress, Physiological Trophoblasts - metabolism Trophoblasts - pathology Ultrasonography, Prenatal ultrasound imaging Umbilical Arteries - physiopathology unfolded protein response Uterine Artery - diagnostic imaging Uterine Artery - pathology Uterine Artery - physiopathology Vascular Remodeling villi regression villous hypoplasia atherosis failure of physiologic transformation placental inflammation villous hypoplasia apoptosis extravillous trophoblast intraplacental oxygen concentration chorion laeve AKT/mTOR fetal growth restriction reactive oxygen species intervillous space ultrasound imaging electron transport chain fetoplacental weight ratio spiral arteries mitochondria perivillous fibrin deposition placental infarct hemochorial placentation interstitial trophoblast unfolded protein response placental location villi regression placenta oxidative stress
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Abstract	Placental-related fetal growth restriction arises primarily due to deficient remodeling of the uterine spiral arteries supplying the placenta during early pregnancy. The resultant malperfusion induces cell stress within the placental tissues, leading to selective suppression of protein synthesis and reduced cell proliferation. These effects are compounded in more severe cases by increased infarction and fibrin deposition. Consequently, there is a reduction in villous volume and surface area for maternal-fetal exchange. Extensive dysregulation of imprinted and nonimprinted gene expression occurs, affecting placental transport, endocrine, metabolic, and immune functions. Secondary changes involving dedifferentiation of smooth muscle cells surrounding the fetal arteries within placental stem villi correlate with absent or reversed end-diastolic umbilical artery blood flow, and with a reduction in birthweight. Many of the morphological changes, principally the intraplacental vascular lesions, can be imaged using ultrasound or magnetic resonance imaging scanning, enabling their development and progression to be followed in vivo. The changes are more severe in cases of growth restriction associated with preeclampsia compared to those with growth restriction alone, consistent with the greater degree of maternal vasculopathy reported in the former and more extensive macroscopic placental damage including infarcts, extensive fibrin deposition and microscopic villous developmental defects, atherosis of the spiral arteries, and noninfectious villitis. The higher level of stress may activate proinflammatory and apoptotic pathways within the syncytiotrophoblast, releasing factors that cause the maternal endothelial cell activation that distinguishes between the 2 conditions. Congenital anomalies of the umbilical cord and placental shape are the only placental-related conditions that are not associated with maldevelopment of the uteroplacental circulation, and their impact on fetal growth is limited.
AbstractList	Placental-related fetal growth restriction arises primarily due to deficient remodeling of the uterine spiral arteries supplying the placenta during early pregnancy. The resultant malperfusion induces cell stress within the placental tissues, leading to selective suppression of protein synthesis and reduced cell proliferation. These effects are compounded in more severe cases by increased infarction and fibrin deposition. Consequently, there is a reduction in villous volume and surface area for maternal-fetal exchange. Extensive dysregulation of imprinted and nonimprinted gene expression occurs, affecting placental transport, endocrine, metabolic, and immune functions. Secondary changes involving dedifferentiation of smooth muscle cells surrounding the fetal arteries within placental stem villi correlate with absent or reversed end-diastolic umbilical artery blood flow, and with a reduction in birthweight. Many of the morphological changes, principally the intraplacental vascular lesions, can be imaged using ultrasound or magnetic resonance imaging scanning, enabling their development and progression to be followed in vivo. The changes are more severe in cases of growth restriction associated with preeclampsia compared to those with growth restriction alone, consistent with the greater degree of maternal vasculopathy reported in the former and more extensive macroscopic placental damage including infarcts, extensive fibrin deposition and microscopic villous developmental defects, atherosis of the spiral arteries, and noninfectious villitis. The higher level of stress may activate proinflammatory and apoptotic pathways within the syncytiotrophoblast, releasing factors that cause the maternal endothelial cell activation that distinguishes between the 2 conditions. Congenital anomalies of the umbilical cord and placental shape are the only placental-related conditions that are not associated with maldevelopment of the uteroplacental circulation, and their impact on fetal growth is limited.Placental-related fetal growth restriction arises primarily due to deficient remodeling of the uterine spiral arteries supplying the placenta during early pregnancy. The resultant malperfusion induces cell stress within the placental tissues, leading to selective suppression of protein synthesis and reduced cell proliferation. These effects are compounded in more severe cases by increased infarction and fibrin deposition. Consequently, there is a reduction in villous volume and surface area for maternal-fetal exchange. Extensive dysregulation of imprinted and nonimprinted gene expression occurs, affecting placental transport, endocrine, metabolic, and immune functions. Secondary changes involving dedifferentiation of smooth muscle cells surrounding the fetal arteries within placental stem villi correlate with absent or reversed end-diastolic umbilical artery blood flow, and with a reduction in birthweight. Many of the morphological changes, principally the intraplacental vascular lesions, can be imaged using ultrasound or magnetic resonance imaging scanning, enabling their development and progression to be followed in vivo. The changes are more severe in cases of growth restriction associated with preeclampsia compared to those with growth restriction alone, consistent with the greater degree of maternal vasculopathy reported in the former and more extensive macroscopic placental damage including infarcts, extensive fibrin deposition and microscopic villous developmental defects, atherosis of the spiral arteries, and noninfectious villitis. The higher level of stress may activate proinflammatory and apoptotic pathways within the syncytiotrophoblast, releasing factors that cause the maternal endothelial cell activation that distinguishes between the 2 conditions. Congenital anomalies of the umbilical cord and placental shape are the only placental-related conditions that are not associated with maldevelopment of the uteroplacental circulation, and their impact on fetal growth is limited. Placental-related fetal growth restriction arises primarily due to deficient remodeling of the uterine spiral arteries supplying the placenta during early pregnancy. The resultant malperfusion induces cell stress within the placental tissues, leading to selective suppression of protein synthesis and reduced cell proliferation. These effects are compounded in more severe cases by increased infarction and fibrin deposition. Consequently, there is a reduction in villous volume and surface area for maternal-fetal exchange. Extensive dysregulation of imprinted and nonimprinted gene expression occurs, affecting placental transport, endocrine, metabolic, and immune functions. Secondary changes involving dedifferentiation of smooth muscle cells surrounding the fetal arteries within placental stem villi correlate with absent or reversed end-diastolic umbilical artery blood flow, and with a reduction in birthweight. Many of the morphological changes, principally the intraplacental vascular lesions, can be imaged using ultrasound or magnetic resonance imaging scanning, enabling their development and progression to be followed in vivo. The changes are more severe in cases of growth restriction associated with preeclampsia compared to those with growth restriction alone, consistent with the greater degree of maternal vasculopathy reported in the former and more extensive macroscopic placental damage including infarcts, extensive fibrin deposition and microscopic villous developmental defects, atherosis of the spiral arteries, and noninfectious villitis. The higher level of stress may activate proinflammatory and apoptotic pathways within the syncytiotrophoblast, releasing factors that cause the maternal endothelial cell activation that distinguishes between the 2 conditions. Congenital anomalies of the umbilical cord and placental shape are the only placental-related conditions that are not associated with maldevelopment of the uteroplacental circulation, and their impact on fetal growth is limited.
Author	Burton, Graham J. Jauniaux, Eric
Author_xml	– sequence: 1 givenname: Graham J. surname: Burton fullname: Burton, Graham J. email: gjb2@cam.ac.uk organization: Center for Trophoblast Research, Department of Physiology, Development, and Neuroscience, University of Cambridge, Cambridge, United Kingdom – sequence: 2 givenname: Eric surname: Jauniaux fullname: Jauniaux, Eric organization: EGA Institute for Women’s Health, Faculty of Population Health Sciences, University College London, London, United Kingdom
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/29422210$$D View this record in MEDLINE/PubMed
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Snippet	Placental-related fetal growth restriction arises primarily due to deficient remodeling of the uterine spiral arteries supplying the placenta during early...
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SubjectTerms	AKT/mTOR apoptosis atherosis chorion laeve Chorionic Villi - metabolism Chorionic Villi - pathology Chorionic Villi - physiopathology electron transport chain extravillous trophoblast failure of physiologic transformation Female fetal growth restriction Fetal Growth Retardation - etiology Fetal Growth Retardation - metabolism Fetal Growth Retardation - physiopathology fetoplacental weight ratio Gene Expression Regulation Genomic Imprinting hemochorial placentation Humans interstitial trophoblast intervillous space intraplacental oxygen concentration Magnetic Resonance Imaging Maternal-Fetal Exchange mitochondria oxidative stress perivillous fibrin deposition placenta Placenta - diagnostic imaging Placenta - pathology Placental Circulation placental infarct placental inflammation Placental Insufficiency - diagnostic imaging Placental Insufficiency - metabolism Placental Insufficiency - pathology Placental Insufficiency - physiopathology placental location Placentation Pre-Eclampsia - metabolism Pre-Eclampsia - physiopathology Pregnancy reactive oxygen species spiral arteries Stress, Physiological Trophoblasts - metabolism Trophoblasts - pathology Ultrasonography, Prenatal ultrasound imaging Umbilical Arteries - physiopathology unfolded protein response Uterine Artery - diagnostic imaging Uterine Artery - pathology Uterine Artery - physiopathology Vascular Remodeling villi regression villous hypoplasia
Title	Pathophysiology of placental-derived fetal growth restriction
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