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      Preeclampsia, of mice and women

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      Physiological Genomics
      American Physiological Society

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          Abstract

          Preeclampsia (PE) is a devastating disorder of pregnancy that affects up to 8% of pregnant women in the United States. The diagnosis of PE is made by the presentation of new-onset hypertension, ≥140 mmHg systolic blood pressure (BP) or ≥90 mmHg diastolic BP, and either proteinuria or another accompanying sign/symptom, such as renal insufficiency, thrombocytopenia, hepatic dysfunction, pulmonary edema, or cerebral/visual. These signs can occur suddenly and without warning. PE that presents before 34 wk of gestation is considered early onset and carries a greater risk for perinatal morbidity/mortality than late-onset PE that occurs at or after 34 wk of gestation. At this time there is no cure for PE, and the only effective treatment is delivery of the baby and placenta. If allowed to progress to eclampsia (PE with neurologic involvement), seizures will occur and possibly death through stroke. PE also carries the risk of significant fetal and neonatal morbidity/mortality in addition to long-term health risks for mother and child. Despite significant research efforts to accurately predict, diagnose, and treat PE, a cure eludes us. Elucidating the pathophysiological mechanisms that can cause PE will aid in our ability to accurately prevent, manage, and treat PE to avoid maternal and fetal losses. Intense research efforts are focused on PE, and the mouse has proven to be a useful animal model for investigating molecular mechanisms that may hold the key to unraveling the mysteries of PE in women.

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          Most cited references47

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          Cardiovascular sequelae of preeclampsia/eclampsia: a systematic review and meta-analyses.

          Preeclampsia affects 3% to 5% of gestations and eclampsia 0.05% to 0.93%, but their subsequent cardiovascular sequelae are unclear. The aim of this study was to determine if women with a history of preeclampsia/eclampsia are at increased risk of long-term cardiovascular sequelae. From Medline and Embase searches, we included case-control and cohort studies that examined cardiac, cerebrovascular or peripheral arterial disease, or cardiovascular mortality>6 weeks postpartum, in women with and without a history of preeclampsia/eclampsia and that controlled for or matched for confounders. Two independent reviewers determined study eligibility and extracted data. Five case-control and 10 cohort studies met eligibility criteria, with a total of 116,175 women with and 2,259,576 women without preeclampsia/eclampsia. Most studies focused on women<56 years of age. Relative to women with uncomplicated pregnancies, women with a history of preeclampsia/eclampsia had an increased risk of subsequent cardiac disease in both the case-control studies (odds ratio 2.47, 95% CI 1.22-5.01) and the cohort studies (relative risk [RR] 2.33, 1.95-2.78), as well as an increased risk of cerebrovascular disease (RR 2.03, 1.54-2.67), peripheral arterial disease (RR 1.87, 0.94-3.73), and cardiovascular mortality (RR 2.29, 1.73-3.04). Meta-regression revealed a graded relationship between the severity of preeclampsia/eclampsia and the risk of cardiac disease (mild: RR 2.00, 1.83-2.19, moderate: RR 2.99, 2.51-3.58, severe: RR 5.36, 3.96-7.27, P<.0001). Women with a history of preeclampsia/eclampsia have approximately double the risk of early cardiac, cerebrovascular, and peripheral arterial disease, and cardiovascular mortality. Further research is needed to determine the mechanisms underlying these associations and to identify effective prevention strategies.
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            Preeclampsia: recent insights.

            Preeclampsia is a pregnancy complication with serious consequences for mother and infant. The disorder is diagnosed by gestational hypertension and proteinuria but is far more than pregnancy induced hypertension. Preeclampsia is proposed to occur in 2 stages. Stage 1 reduced placental perfusion is postulated as the root cause and to lead to the maternal syndrome, Stage 2. Why perfusion is reduced, how this translates to a maternal disease in some but not all women and what is the linkage of the 2 stages are topics of intense study. In the last decade such studies have provided valuable insights into pathophysiology that now guide ongoing clinical trials.
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              Placental stress and pre-eclampsia: a revised view.

              In pre-eclampsia, poor placentation causes both oxidative and endoplasmic reticulum stress of the placenta. It is believed placental hypoxia stimulates excessive production of soluble fms-like tyrosine kinase 1 (sFlt-1), which binds and deactivates circulating vascular endothelial growth factor (VEGF). When maternal endothelium is deprived of VEGF it becomes dysfunctional hence leading to the clinical syndrome of the mother. In this paper the previous claim that poor placentation may predispose more to placental oxidative stress than hypoxia is reiterated. We show why pre-eclampsia is not only an endothelial disease, but also a disorder of systemic inflammation. We question that hypoxia is the only or indeed the main stimulus to release of sFlt-1; and emphasise the role of inflammatory mechanisms. Hypoxia cannot be assumed simply because hypoxia-inducible transcription factors (HIF) are upregulated. Concurrent assessments of nuclear factor-kappaB (NF-kappaB), a transcription factor for inflammatory responses are desirable to obtain a more complete picture. We point out that the pre-eclampsia placenta is the source of bioactive circulating factors other than sFlt-1 in concentrations that are much higher than in normal pregnancy. These may also contribute to the final inflammatory syndrome. We propose a modified version of the two-stage model for pre-eclampsia.
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                Author and article information

                Journal
                Physiological Genomics
                Physiological Genomics
                American Physiological Society
                1094-8341
                1531-2267
                August 2016
                August 2016
                : 48
                : 8
                : 565-572
                Article
                10.1152/physiolgenomics.00125.2015
                5005458
                27260843
                64c32228-6af0-4861-895e-7dfc66a6e396
                © 2016
                History

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