ArticleScientific reports2019
Long-term cardiovascular disorders in the STOX1 mouse model of preeclampsia.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Reduced circulating STOX1 is associated with inflammatory cytokines and insulin resistance in obese individuals: a cross-sectional study.Frontiers in nutrition · 2026Article
- Overexpression of the STOX1B isoform of STOX1 triggers preeclampsia-like symptoms through HNF4α-dependent alterations of coagulation cascades in mice.Scientific reports · 2025Article
- Article
- Maternal Microvascular Dysfunction During and After Preeclamptic Pregnancy.Comprehensive Physiology · 2024Review
- Metabolic theory of preeclampsia: implications for maternal cardiovascular health.American journal of physiology. Heart and circulatory physiology · 2024Review
- Early- to mid-gestational testosterone excess leads to adverse cardiac outcomes in postpartum sheep.American journal of physiology. Heart and circulatory physiology · 2024Article
- Differences in Cardiometabolic Proteins in Pregnancy Prioritize Relevant Targets of Preeclampsia.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Linking genotype to trophoblast phenotype in preeclampsia and HELLP syndrome associated withiScience · 2024Article
- RISING STARS: Approaches to modeling placental function in preeclampsia in vitro and in vivo.The Journal of endocrinology · 2023Article
- The Clinical Value of Rodent Models in Understanding Preeclampsia Development and Progression.Current hypertension reports · 2023Review
- Impact of Adverse Gestational Milieu on Maternal Cardiovascular Health.Endocrinology · 2023Review
- Pathophysiological impact of CXC and CX3CL1 chemokines in preeclampsia and gestational diabetes mellitus.Frontiers in cell and developmental biology · 2023Review
- Preeclampsia and Fetal Growth Restriction as Risk Factors of Future Maternal Cardiovascular Disease-A Review.Journal of clinical medicine · 2022Review
- The L-NAME mouse model of preeclampsia and impact to long-term maternal cardiovascular health.Life science alliance · 2022Article
- Article
- Animal Models of Cardiovascular Complications of Pregnancy.Circulation research · 2022Review
- Can Diagnostic Specificity and Phenotyping Aid in Evaluating Cardiometabolic Risk of Maternal Sleep-disordered Breathing?American journal of respiratory and critical care medicine · 2022Article
- Animal models of preeclampsia: investigating pathophysiology and therapeutic targets.American journal of obstetrics and gynecology · 2022Review
- Pregnancy, preeclampsia and maternal aging: From epidemiology to functional genomics.Ageing research reviews · 2022Review
- NRP1 and MMP9 are dual targets of RNA-binding protein QKI5 to alter VEGF-R/ NRP1 signalling in trophoblasts in preeclampsia.Journal of cellular and molecular medicine · 2021Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adverse long-term cardiovascular (CV) consequences of PE are well established in women. However, the mechanism responsible for that risk remains unknown. Here, we mated wild-type female mice of the FVB/N strain to STOX1A-overexpressing mice to mimic severe PE and investigated the long-term consequences on the maternal cardiovascular system. Ultrasonography parameters were analyzed in mice before pregnancy and at 3 and 6 months post-pregnancy. At 6 months post-pregnancy, cardiac stress test induced by dobutamine injection revealed an abnormal ultrasonography Doppler profile in mice with previous PE. Eight months post-pregnancy, the heart, endothelial cells (ECs) and plasma of females were analyzed and compared to controls. The heart of mice with PE showed left-ventricular hypertrophy associated with altered histology (fibrosis). Transcriptomic analysis revealed the deregulation of 1149 genes in purified ECs and of 165 genes in the hearts, many being involved in heart hypertrophy. In ECs, the upregulated genes were associated with inflammation and cellular stress. Systems biology analysis identified interleukin 6 (IL-6) as a hub gene connecting these pathways. Plasma profiling of 33 cytokines showed that, 8 of them (Cxcl13, Cxcl16, Cxcl11, IL-16, IL-10, IL-2, IL-4 and Ccl1) allowed to discriminate mice with previous PE from controls. Thus, PE triggers female long-term CV consequences on the STOX1 mouse model.
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