Preeclampsia and Cardiovascular Risk for Offspring

Wojczakowski, Wiktor; Kimber-Trojnar, Żaneta; Dziwisz, Filip; Słodzińska, Magdalena; Słodziński, Hubert; Leszczyńska‐Gorzelak, Bożena

doi:10.3390/jcm10143154

Cited by 30 publications

(28 citation statements)

References 159 publications

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“…Offspring of hypoxic pregnancies display cardiac abnormalities in adulthood and appear to be sensitized to ischemia/reperfusion injury 7,9–17 . These findings support epidemiological evidence from human pregnancies, which show hypoxia during development can increase the risk of cardiac dysfunction in offspring 18–23 . Combined, evidence derived from human clinical studies and from experimental preclinical models strongly supports that fetal hypoxia is an independent risk factor for offspring cardiovascular disease.…”

Section: Introductionsupporting

confidence: 68%

“…7,[9][10][11][12][13][14][15][16][17] These findings support epidemiological evidence from human pregnancies, which show hypoxia during development can increase the risk of cardiac dysfunction in offspring. [18][19][20][21][22][23] Combined, evidence derived from human clinical studies and from experimental preclinical models strongly supports that fetal hypoxia is an independent risk factor for offspring cardiovascular disease. Understanding the factors that drive cardiac dysfunction in hypoxic pregnancies provides an exciting opportunity to develop therapeutics that prevent abnormal developmental programming of cardiovascular disease.…”

Section: Introductionmentioning

confidence: 97%

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Chronic developmental hypoxia alters mitochondrial oxidative capacity and reactive oxygen species production in the fetal rat heart in a sex‐dependent manner

Smith

Swiderska

Lock

et al. 2022

Journal of Pineal Research

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Insufficient oxygen supply (hypoxia) during fetal development leads to cardiac remodeling and a predisposition to cardiovascular disease in later life. Previous work has shown hypoxia causes oxidative stress in the fetal heart and alters the activity and expression of mitochondrial proteins in a sex‐dependent manner. However, the functional effects of these modifications on mitochondrial respiration remain unknown. Furthermore, while maternal antioxidant treatments are emerging as a promising new strategy to protect the hypoxic fetus, whether these treatments convey similar protection to cardiac mitochondria in the male or female fetus has not been investigated. Therefore, using an established rat model, we measured the sex‐dependent effects of gestational hypoxia and maternal melatonin treatment on fetal cardiac mitochondrial respiration, reactive oxygen species (ROS) production, and lipid peroxidation. Pregnant Wistar rats were subjected to normoxia or hypoxia (13% oxygen) during gestational days (GDs) 6–20 (term ~22 days) with or without melatonin treatment (5 µg/ml in maternal drinking water). On GD 20, mitochondrial aerobic respiration and H2O2 production were measured in fetal heart tissue, together with lipid peroxidation and citrate synthase (CS) activity. Gestational hypoxia reduced maternal body weight gain (p < .01) and increased placental weight (p < .05) but had no effect on fetal weight or litter size. Cardiac mitochondria from male but not female fetuses of hypoxic pregnancy had reduced respiratory capacity at Complex II (CII) (p < .05), and an increase in H2O2 production/O2 consumption (p < .05) without any changes in lipid peroxidation. CS activity was also unchanged in both sexes. Despite maternal melatonin treatment increasing maternal and fetal plasma melatonin concentration (p < .001), melatonin treatment had no effect on any of the mitochondrial parameters investigated. To conclude, we show that gestational hypoxia leads to ROS generation from the mitochondrial electron transport chain and affects fetal cardiac mitochondrial respiration in a sex‐dependent manner. We also show that maternal melatonin treatment had no effect on these relationships, which has implications for the development of future therapies for hypoxic pregnancies.

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Section: Introductionsupporting

confidence: 68%

Section: Introductionmentioning

confidence: 97%

Chronic developmental hypoxia alters mitochondrial oxidative capacity and reactive oxygen species production in the fetal rat heart in a sex‐dependent manner

Smith

Swiderska

Lock

et al. 2022

Journal of Pineal Research

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“…It should be mentioned that NO synthase inhibition is an established animal model of preeclampsia [25,26]. In our study, pregnant females supplemented with L-NAME have common symptoms of human preeclampsia, such as arterial hypertension, a decrease in the blood content of nitric oxide metabolites, and intrauterine growth restriction of the offspring [21][22][23]. Therefore, our findings could be useful for understanding the mechanisms of cardiovascular disorders in the offspring produced under conditions of maternal preeclampsia.…”

Section: Discussionmentioning

confidence: 65%

“…In contrast, NO deficiency delays sympathetic innervation development. Importantly, a decrease in NO bioavailability in the developing organism may be the result of maternal preeclampsia [20,21], which affects up to 5% of all pregnancies and has adverse outcomes on the offspring circulatory system [22,23]. In particular, neonatal arterial hypotension is common in infants born from preeclamptic mothers [24], although it is not yet clear whether this is due to the underdevelopment of sympathetic vascular control.…”

Section: Introductionmentioning

confidence: 99%

Intrauterine L-NAME Exposure Weakens the Development of Sympathetic Innervation and Induces the Remodeling of Arterial Vessels in Two-Week-Old Rats

Selivanova

Shvetsova

Борзых

et al. 2021

IJMS

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Nitric oxide (NO) has been shown to stimulate differentiation and increase the survival of ganglionic sympathetic neurons. The proportion of neuronal NOS-immunoreactive sympathetic preganglionic neurons is particularly high in newborn rats and decreases with maturation. However, the role of NO in the development of vascular sympathetic innervation has never been studied before. We tested the hypothesis that intrauterine NO deficiency weakened the development of vascular sympathetic innervation and thereby changed the contractility of peripheral arteries and blood pressure level in two-week-old offspring. Pregnant rats consumed NOS inhibitor L-NAME (250 mg/L in drinking water) from gestational day 10 until delivery. Pups in the L-NAME group had a reduced body weight and blood level of NO metabolites at 1–2 postnatal days. Saphenous arteries from two-week-old L-NAME offspring demonstrated a lower density of sympathetic innervation, a smaller inner diameter, reduced maximal active force and decreased α-actin/β-actin mRNA expression ratio compared to the controls. Importantly, pups in the L-NAME group exhibited decreased blood pressure levels before, but not after, ganglionic blockade with chlorisondamine. In conclusion, intrauterine L-NAME exposure is followed by the impaired development of the sympathetic nervous system in early postnatal life, which is accompanied by the structural and functional remodeling of arterial blood vessels.

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“…Preeclampsia is a relevant issue in obstetrics, affecting 2–8% of pregnancies worldwide. It is one of the most common causes of morbidity and mortality in the perinatal period of mothers and their offspring [ 42 , 43 , 44 , 45 , 46 ]. The mechanism of preeclampsia is yet to be fully understood.…”

Section: Gut Microbiome and Preeclampsiamentioning

confidence: 99%

Changes in the Gut Microbiome and Pathologies in Pregnancy

GORCZYCA

Obuchowska

Kimber-Trojnar

et al. 2022

IJERPH

Self Cite

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Pregnancy is a special period in a woman’s life when her organism undergoes multiple physiological changes so that the fetus has optimal conditions for growth and development. These include modifications in the composition of the microbiome that occur between the first and third trimesters of pregnancy. There is an increase in Akkermansia, Bifidobacterium, and Firmicutes, which have been associated with an increase in the need for energy storage. The growth in Proteobacteria and Actinobacteria levels has a protective effect on both the mother and the fetus via proinflammatory mechanisms. The aim of the study is to review the research on the relationship between the mother’s intestinal microbiome and gestational pathologies. Changes in the maternal gut microbiome is probably one of the mechanisms that occurs in various pregnancy diseases such as preeclampsia, fetal growth restriction, gestational diabetes mellitus, excessive gestational weight gain, and premature birth. For this reason, it seems vital to pay attention to certain interventions that can benefit the affected patients both in the short term, by preventing complications during pregnancy, and in the long term, as one of the mechanisms occurring in various gestational diseases is dysbiosis of the maternal intestinal flora.

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Preeclampsia and Cardiovascular Risk for Offspring

Cited by 30 publications

References 159 publications

Chronic developmental hypoxia alters mitochondrial oxidative capacity and reactive oxygen species production in the fetal rat heart in a sex‐dependent manner

Chronic developmental hypoxia alters mitochondrial oxidative capacity and reactive oxygen species production in the fetal rat heart in a sex‐dependent manner

Intrauterine L-NAME Exposure Weakens the Development of Sympathetic Innervation and Induces the Remodeling of Arterial Vessels in Two-Week-Old Rats

Changes in the Gut Microbiome and Pathologies in Pregnancy

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