Preeclampsia and Fetal Growth Restriction as Risk Factors of Future Maternal Cardiovascular Disease—A Review

Sławek-Szmyt, Sylwia; Kawka-Paciorkowska, Katarzyna; Ciepłucha, Aleksandra; Lesiak, Maciej; Ropacka-Lesiak, Mariola

doi:10.3390/jcm11206048

Cited by 10 publications

(8 citation statements)

References 130 publications

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“…Our preliminary results are consistent with the previous reports about the cardiovascular system in healthy pregnant women, particularly in the context of the left ventricular global strain [7,8]. The other echocardiographic data are within the normal range.…”

Section: Preliminary Results and Discussionsupporting

confidence: 92%

Maladaptation of the maternal cardiovascular system as a cause of fetal growth restriction: Study rationale and design

et al. 2022

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Section: Preliminary Results and Discussionsupporting

confidence: 92%

Maladaptation of the maternal cardiovascular system as a cause of fetal growth restriction: Study rationale and design

et al. 2022

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“…It is speculated that abnormal upregulation of GPR65 leads to insufficient remodeling of spiral arteries in trophoblast cells, which leads to the occurrence and development of PE. Uterine and placental dysfunction caused by preeclampsia may develop clinically into fetal growth restriction [ 57 ]. Therefore, further investigation into the molecular mechanisms by which GPR65 regulates trophoblast cells under hypoxic conditions will contribute to a better understanding of the pathogenesis of these diseases and may provide novel insights for the treatment of preeclampsia and fetal growth restriction.…”

Section: Discussionmentioning

confidence: 99%

GPR65 inhibits human trophoblast cell adhesion through upregulation of MYLK and downregulation of fibronectin via cAMP-ERK signaling in a low pH environment

Mao,

Feng,

Zheng

et al. 2023

Cell Commun Signal

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Background Extravillous trophoblasts (EVTs) are essential cells during the formation of the placenta, with the major function of invading the maternal decidua, anchoring the developing placenta to the uterus, remodeling uterine arteries, and regulating immune responses to prevent rejection. During early pregnancy, the decidua undergoes a hypoxic and acidic microenvironment, which has been shown to participate in tumor cell migration, invasion, growth, and angiogenesis. Nevertheless, the mechanisms by which EVTs sense and respond to the acidic microenvironment, thereby executing their functions, remain poorly understood. Methods The effects of G protein-coupled receptor 65 (GPR65) on cell adhesion and other cellular functions were tested using JAR spheroids, mouse blastocysts, and HTR-8/SVneo cells. Specifically, we employed HTR-8/SVneo cells for gene overexpression and silencing to investigate the underlying mechanism of GPR65's impact on trophoblast cell function under acidic conditions. Additionally, villus tissue samples obtained from early pregnancy loss patients were utilized to explore the potential association between GPR65 and its related signaling pathway molecules with the disease. Results This study identified GPR65 expression widely in trophoblasts, with the highest level in EVTs. Importantly, optimal GPR65 levels are required for maintaining normal adhesion, migration, and invasion, whereas overexpression of GPR65 inhibits these functions by activating the cAMP-ERK signaling pathway, upregulating myosin light chain kinase (MYLK) and MYLK3 expression, and subsequently downregulating fibronectin. Consistently, elevated expression of GPR65, MYLK, and MYLK3 is observed in patients suffering from early pregnancy loss. Conclusions This work offers insights into the suppressive effects of GPR65 on EVT function under acidic conditions and highlights a putative target for therapeutic intervention in early pregnancy complications.

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“…Almost three quarters of the cohort had a cesarean section, which is associated with more complications than vaginal birth for the current pregnancy and future pregnancies [18]. 21% of the women gave birth to a newborn with intrauterine growth restriction which is in itself a cardiovascular risk factor offspring later in life [19]. This aspect of HDP and PPHT is again associated with poor outcomes [20].…”

Section: Discussionmentioning

confidence: 99%

Protocol and Characteristics of the Basel Postpartum Hypertension Cohort (Basel-PPHT-Cohort): an Interim Analysis

Socrates,

Wenker,

Vischer

et al. 2024

Preprint

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Introduction: Postpartum hypertension (PPHT) is hypertension that persists or develops directly after pregnancy. PPHT affects 10% of pregnancies and is the most common cause for re-hospitalization after giving birth. In general, PPHT stems from hypertensive disorders of pregnancy (HDP). The aim of the current interim report of the Basel PPHT registry is to describe the cohort, and to determine feasibility and acceptance of a home-based telemonitoring management strategy (HBTMS) in women with PPHT. Methods: Enrollment in the cohort began in June 2020 during the SARS-CoV-2 pandemic at the University Hospital Basel. Women in the maternity ward were screened for preexisting hypertension, HDP, and de novo postpartum hypertension and after consenting, were enrolled. In this pragmatic non-randomized prospective trial, women in the PPHT cohort could choose, between a HBTMS or usual care which consisted of in-hospital appointments at the hypertension clinic. HBTMS was defined as a smartphone application or a programmed spreadsheet to report blood pressure followed by telephone consultations. Standard of care was hospital-based visits as clinically needed after discharge. All participants were assessed three months after delivery with a standardized clinical visit including a 24-hour blood pressure measurement, blood, biomarker, and urine analysis. Results: 311 participants were enrolled from 06/20-08/23. Mean age was 34±5.3 years. Regarding pregnancy-related medical history: 10 % had preexisting hypertension, 27.3 % gestational hypertension, 53% preeclampsia (PE), 0.3% eclampsia, 6% HELLP (Hemolysis, Elevated Liver enzymes and Low Platelets) and 18.3% had de novo PPHT. More than one diagnosis was possible. Family history of cardiovascular disease was seen in 49.5%, 7.5% had a family history of PE. 23.3% were determined as high risk for PE during pregnancy. The most common type of delivery was C-Section (68.5%), mean hospital stay was 6.3 days (±3.9) and IUGR (intrauterine growth restriction) was seen in 21% of the newborns. 99% of participants chose a home-based management strategy. Conclusion: This first description of the Basel PPHT Cohort showed that a HBTMS is well accepted. This is particularly relevant in the direct postpartum period and even more pertinent when the exposure of hospital visits should be avoided when possible.

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Preeclampsia and Fetal Growth Restriction as Risk Factors of Future Maternal Cardiovascular Disease—A Review

Cited by 10 publications

References 130 publications

Maladaptation of the maternal cardiovascular system as a cause of fetal growth restriction: Study rationale and design

Maladaptation of the maternal cardiovascular system as a cause of fetal growth restriction: Study rationale and design

GPR65 inhibits human trophoblast cell adhesion through upregulation of MYLK and downregulation of fibronectin via cAMP-ERK signaling in a low pH environment

Protocol and Characteristics of the Basel Postpartum Hypertension Cohort (Basel-PPHT-Cohort): an Interim Analysis

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