Physiopathology of late-onset fetal growth restriction

Júnior, Edward Araujo; Zamarian, Ana Cristina Perez; Caetano, Ana Carolina Rabachini; Peixoto, Alberto Borges; Nardozza, Luciano Marcondes Machado

doi:10.23736/s2724-606x.21.04771-7

Cited by 8 publications

(5 citation statements)

References 58 publications

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“…10,11 During pregnancy, alterations in uterine spiral artery remodeling could lead to the reduction of placental circulation and placental ischemia, ultimately resulting in abnormal fetal development. 12–14 In a similar study, the fetuses with higher survival and better intrauterine growth are always consistent with a denser placental vascular network. 15 Our previous studies also observed poor placental angiogenesis in low-birth-weight fetuses.…”

mentioning

confidence: 61%

Adenosine-ADORA2A Promotes Ang-Induced Angiogenesis in Intrauterine Growth Restriction Placenta via the Stat3/Akt Pathway

Xiang

Feng

et al. 2023

ATVB

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BACKGROUND: Abnormal placental angiogenesis is an important cause of fetal intrauterine growth restriction (IUGR), but its underlying mechanisms and therapies remain unclear. Adenosine and its mediated signaling has been reported to be associated with the development of angiogenesis. However, whether the adenosine-related signaling plays a role in modulating angiogenesis in placenta and the IUGR pregnancy outcomes remains unclear. METHODS: The angiogenesis and adenosine signaling expressions in normal and IUGR placentas were detected in different species. And the role of adenosine in regulating IUGR pregnancy outcomes was evaluated using diet-induced IUGR mouse model. Molecular mechanisms underlying adenosine-induced angiogenesis were investigated by in vitro angiogenesis assays and in vivo Matrigel plug assays. RESULTS: Here, we demonstrated poor angiogenesis and low adenosine concentration and downregulated expression of its receptor A2a (ADORA2A [adenosine A2a receptor]) in IUGR placenta. Additionally, the beneficial effects of adenosine in improving IUGR pregnancy outcomes were revealed in a diet-induced IUGR mouse model. Moreover, adenosine was found to effectively improve adenosine signaling and angiogenesis in IUGR mice placenta. Mechanistically, by using angiogenesis assays in vitro and in vivo, adenosine was shown to activate ADORA2A to promote the phosphorylation of Stat3 (signal transducer and activator of transcription 3) and Akt (protein kinase B), resulting in increased Ang (angiogenin)-dependent angiogenesis. CONCLUSIONS: Collectively, this study uncovers an unexpected mechanism of promoting placental angiogenesis by adenosine-ADORA2A signaling and advances the translation of this signaling as a prognostic indicator and therapeutic target in IUGR treatment.

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mentioning

confidence: 61%

Adenosine-ADORA2A Promotes Ang-Induced Angiogenesis in Intrauterine Growth Restriction Placenta via the Stat3/Akt Pathway

Xiang

Feng

et al. 2023

ATVB

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“…Placental factors are released into maternal circulation from the early stages of placentation, and some factors change with altered placental growth, function and impaired oxygenation and/or damage to the placenta (Araujo Junior et al, 2021). A recent metabolomic study demonstrated high predictive accuracy for FGR with a combination of 3-hydroxybutyric acid, glycine and phosphatidylcholine with acyl-alkyl residue C42 (Bahado-Singh et al, 2022).…”

Section: Plasma and Maternal Cardiovascular And Serum Biomarkersmentioning

confidence: 99%

Fetal growth restriction and stillbirth: Biomarkers for identifying at risk fetuses

et al. 2022

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Fetal growth restriction (FGR) is a major cause of stillbirth, prematurity and impaired neurodevelopment. Its etiology is multifactorial, but many cases are related to impaired placental development and dysfunction, with reduced nutrient and oxygen supply. The fetus has a remarkable ability to respond to hypoxic challenges and mounts protective adaptations to match growth to reduced nutrient availability. However, with progressive placental dysfunction, chronic hypoxia may progress to a level where fetus can no longer adapt, or there may be superimposed acute hypoxic events. Improving detection and effective monitoring of progression is critical for the management of complicated pregnancies to balance the risk of worsening fetal oxygen deprivation in utero, against the consequences of iatrogenic preterm birth. Current surveillance modalities include frequent fetal Doppler ultrasound, and fetal heart rate monitoring. However, nearly half of FGR cases are not detected in utero, and conventional surveillance does not prevent a high proportion of stillbirths. We review diagnostic challenges and limitations in current screening and monitoring practices and discuss potential ways to better identify FGR, and, critically, to identify the “tipping point” when a chronically hypoxic fetus is at risk of progressive acidosis and stillbirth.

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“…Ведущая роль в патогенезе связанных с гипергликемией осложнений беременности принадлежит микроциркуляторным нарушениям [9]. Оксидативный стресс, индуцированный в ишемизированной плаценте, сопровождается активацией апоптоза, дисфункцией эндотелия (ДЭ) с возможным развитием плацентарной недостаточности (ПН) [10][11][12][13][14]. Нарушение аутокринных регуляторных про-и антиангиогенных факторов при ГСД обусловливает структурное ремоделирование сосудистого русла, развитие ангиопатий, что в конечном счете может привести к формированию ПН, нарушению маточно-плацентарного кровотока (НМПК), задержке роста плода (ЗРП) [15].…”

Section: Introductionunclassified

Pregnancy course and outcomes in patients with non-insulin dependent gestational diabetes mellitus: An observational cohort study

Sytykh,

Putilova

2024

Kuban. nauсh. med. vestnik

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Background. Gestational diabetes mellitus is the most frequent metabolic disorder during pregnancy. Its prevalence is steadily increasing worldwide. In the setting of hyperinsulinism, this pathology may cause various structural and functional changes in the placenta, as well as a reduction in oxygen supply to the fetus. This may result in fetal hypoxia and increased risk of fetal growth restriction. Therefore, research into the specific features of gestation course in patients with gestational diabetes mellitus in order to prevent its complications appears relevant. Objective. To study the specific features of gestation, delivery, and perinatal outcomes in patients with non-insulin dependent gestational diabetes mellitus. Methods. We conducted an observational cohort study of the case histories of 120 women with singleton pregnancies of the second and third trimesters with diagnosed non-insulin dependent gestational diabetes mellitus, their labor and delivery records, and the medical records of the newborns. All the patients were managed at the Ural Research Institute of Maternity and Child Care during 2021–2023. The main group comprised 70 patients whose pregnancy was complicated by sub- and decompensated forms of placental insufficiency. The comparison group comprised 50 pregnant women without pathologies of the fetoplacental complex. The obstetric history, gestation course of the present pregnancy and its outcomes, as well as the condition of the newborns, were analyzed. The obtained data were processed by the methods of variation statistics using Microsoft Excel spreadsheets (Microsoft, USA) and Statistica 13 (DellInc., USA) and MedCalc 15.8 (MedCalcSoftware, Belgium) applications. The null hypothesis was rejected at p > 0.05. Results. Gestational diabetes mellitus in previous pregnancies was statistically significantly less frequent in the main group (2.9% (n = 2)) than in the comparison group (18.0% (n = 9)) ( p > 0.05). Placental insufficiency in the main group was characterized by fetal growth restriction, which was associated with impaired uteroplacental blood flow in 58.6% (n = 41) of the cases. In the main group, the pregnancy ended in preterm delivery in 21.4% (n = 15) of the cases; in 78.6% (n = 55) of the cases, the delivery was at term. There were no preterm births in the comparison group, p > 0.05. Cesarean section was performed in 62.9% (n = 44) of patients in the main group, compared to 20.0% (n = 10) in the comparison group ( p > 0.05). Newborns of the main group required respiratory support more often (p > 0.05). Conclusion. The mechanism of placental insufficiency in patients with non-insulin dependent gestational disorders of carbohydrate metabolism remains to be elucidated. Further research should investigate the predictors of fetoplacental complex pathologies in this group of patients in order to reduce the number of perinatal complications.

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Physiopathology of late-onset fetal growth restriction

Cited by 8 publications

References 58 publications

Adenosine-ADORA2A Promotes Ang-Induced Angiogenesis in Intrauterine Growth Restriction Placenta via the Stat3/Akt Pathway

Adenosine-ADORA2A Promotes Ang-Induced Angiogenesis in Intrauterine Growth Restriction Placenta via the Stat3/Akt Pathway

Fetal growth restriction and stillbirth: Biomarkers for identifying at risk fetuses

Pregnancy course and outcomes in patients with non-insulin dependent gestational diabetes mellitus: An observational cohort study

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