Literature DB >> 30051401

Cardiovascular Sequels During and After Preeclampsia.

Nina D Paauw1, A Titia Lely2.   

Abstract

Preeclampsia is a pregnancy-specific disorder complicating 2%-8% of pregnancies worldwide and characterized by de novo development of hypertension and proteinuria. Current understanding of the pathophysiology of preeclampsia is limited. A main feature is disrupted spiral artery remodeling in the placenta, which restricts the blood flow to the placenta, which in turn leads to decreased uteroplacental perfusion. Impaired blood flow through the placenta might result in fetal growth restriction and secretion of several factors by the placenta-mainly pro-inflammatory cytokines and anti-angiogenic factors-which spread into the maternal circulation, leading to endothelial dysfunction, which subsequently results in disrupted maternal hemodynamics. To date, no treatment options are available apart from termination of pregnancy. Despite normalization of the maternal vascular disturbances after birth, it has become apparent that formerly preeclamptic women experience an increased risk to develop cardiovascular and kidney disease later in life. One well-accepted concept is that the development of preeclampsia is an indicator of maternal susceptibility to develop future cardiovascular conditions, although the increased risk might also be the result of organ damage caused during preeclampsia. Given the associations between preeclampsia and long-term complications, preeclampsia is acknowledged as woman-specific risk factor for cardiovascular disease. Current research focuses on finding effective screening and prevention strategies for the reduction of cardiovascular disease in women with a history of preeclampsia.

Entities:  

Keywords:  Anti-angiogenic factor; Endoglin; Fetal growth restriction; Gestational hypertension; Maternal hemodynamics; Placental dysfunction; Placentation; Preeclampsia; Pro-inflammatory cytokines; Renal function; Renin-angiotensin aldosterone system; Syncytiotrophoblast; Uteroplacental perfusion; s-Flt1

Mesh:

Year:  2018        PMID: 30051401     DOI: 10.1007/978-3-319-77932-4_28

Source DB:  PubMed          Journal:  Adv Exp Med Biol        ISSN: 0065-2598            Impact factor:   2.622


  9 in total

1.  Chronic kidney disease in preeclamptic patients: not found unless searched for-Is a nephrology evaluation useful after an episode of preeclampsia?

Authors:  Zineb Filali Khattabi; Marilisa Biolcati; Antioco Fois; Antoine Chatrenet; Delphine Laroche; Rossella Attini; Marie Therese Cheve; Giorgina Barbara Piccoli
Journal:  J Nephrol       Date:  2019-07-17       Impact factor: 3.902

2.  Multivariate logistic regression analysis of preeclampsia in patients with pregnancy induced hypertension and the risk predictive value of monitoring platelet, coagulation function and thyroid hormone in pregnant women.

Authors:  Li Zeng; Chunfang Liao
Journal:  Am J Transl Res       Date:  2022-09-15       Impact factor: 3.940

3.  The Intersection of Maternal Metabolic Syndrome, Adverse Pregnancy Outcomes, and Future Metabolic Health for the Mother and Offspring.

Authors:  Guillermina Girardi; Andrew A Bremer
Journal:  Metab Syndr Relat Disord       Date:  2022-04-05       Impact factor: 2.363

4.  Circulating endocan and preeclampsia: a meta-analysis.

Authors:  Xia Lan; Zhaoming Liu
Journal:  Biosci Rep       Date:  2020-01-31       Impact factor: 3.840

5.  Maternal cardiovascular disease after twin pregnancies complicated by hypertensive disorders of pregnancy: a population-based cohort study.

Authors:  Liran Hiersch; Joel G Ray; Jon Barrett; Howard Berger; Michael Geary; Sarah D McDonald; Christina Diong; Sima Gandhi; Jun Guan; Beth Murray-Davis; Nir Melamed
Journal:  CMAJ       Date:  2021-09-20       Impact factor: 8.262

6.  Increased LINC00922 in preeclampsia regulates the proliferation, invasion, and migration of placental trophoblast cells.

Authors:  Chengzhen Gao; Hui Yang; Fei Xia
Journal:  Ann Transl Med       Date:  2021-10

7.  LncRNA small nucleolar RNA host gene 5 inhibits trophoblast autophagy in preeclampsia by targeting microRNA-31-5p and promoting the transcription of secreted protein acidic and rich in cysteine.

Authors:  Lei Yang; Chao Liu; Chao Zhang; Ruotian Shang; Yichen Zhang; Shiyuan Wu; Yan Long
Journal:  Bioengineered       Date:  2022-03       Impact factor: 3.269

Review 8.  Current State of Preeclampsia Mouse Models: Approaches, Relevance, and Standardization.

Authors:  Christopher A Waker; Melissa R Kaufman; Thomas L Brown
Journal:  Front Physiol       Date:  2021-07-02       Impact factor: 4.566

9.  Increased FUN14 domain containing 1 (FUNDC1) ubiquitination level inhibits mitophagy and alleviates the injury in hypoxia-induced trophoblast cells.

Authors:  GuoQing Chen; Lu Chen; Yan Huang; XiongShan Zhu; YuanLan Yu
Journal:  Bioengineered       Date:  2022-02       Impact factor: 3.269

  9 in total

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