Review
Medicine, General & Internal
Teresa M. MacDonald, Susan P. Walker, Natalie J. Hannan, Stephen Tong, Tu'uhevaha J. Kaitu'u-Lino
Summary: Preeclampsia is a pregnancy-specific disease that has a significant impact on maternal and perinatal morbidity and mortality worldwide. Currently, there are limited options for predicting and diagnosing preeclampsia, and further research is needed to identify effective tests and biomarkers.
Article
Biochemistry & Molecular Biology
Shanshui Zeng, Yue Pan, Fei Liu, Jiaye Yin, Min Jiang, Yan Long, Xueqin Zhao, Gendie E. Lash, Hongling Yang
Summary: The study found that the expression of CLU is increased before the onset of PE and is positively correlated with the severity of the condition. CLU can inhibit the epithelial-mesenchymal transition of trophoblast cells, thereby reducing cell migration and invasion.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2021)
Review
Biochemistry & Molecular Biology
Mingyu Hu, Ji Li, Philip N. Baker, Chao Tong
Summary: Preeclampsia is a major threat to the health of mothers and newborns worldwide, primarily due to placental metabolic abnormalities leading to placental dysfunction.
Review
Environmental Sciences
Miaoliang Wu, Fuhui Yan, Qian Liu, Ganzhong Liao, Yilin Shen, Zhi Bai, Xiaoshan Liu
Summary: Preeclampsia (PE) is a disease that occurs after 20 weeks of pregnancy and is characterized by new onset hypertension and albuminuria or other end-organ damage. It is a major complication of pregnancy that can increase morbidity and mortality in pregnant women and fetuses, causing significant social burden. Recent research suggests that exposure to environmental xenobiotic compounds, particularly endocrine disruptors, may contribute to the development of PE. However, the specific mechanisms underlying this relationship remain unclear. This paper reviews the role and potential mechanism of PE induced by exogenous chemicals and provides an outlook on the environmental etiology of PE.
Article
Cell Biology
Xiaotong Yang, Paula A. Benny, Elorri Cervera-Marzal, Biyu Wu, Cameron B. Lassiter, Joshua Astern, Lana X. Garmire
Summary: Variations in telomere length have been linked to aging, stress, and diseases. This study investigated the association between placental telomere length and preeclampsia. The results suggest that placental telomere length is not significantly different between severe preeclampsia cases and healthy controls, but it is negatively correlated with gestational age and influenced by race.
Article
Cell Biology
Leonardo Ermini, Abby Farrell, Sruthi Alahari, Jonathan Ausman, Chanho Park, Julien Sallais, Megan Melland-Smith, Tyler Porter, Michael Edson, Ori Nevo, Michael Litvack, Martin Post, Isabella Caniggia
Summary: Aberrant ceramide build-up in preeclampsia leads to exuberant autophagy-mediated trophoblast cell death. Lysosome formation is markedly increased in trophoblast cells of early-onset preeclamptic placentae, accompanied by augmented levels of transcription factor EB. Ceramide-induced lysosomal biogenesis and exocytosis contribute to maternal endothelial dysfunction in preeclampsia.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Review
Cell Biology
Peng Xu, Yeling Ma, Hongyu Wu, Yan-Ling Wang
Summary: Disorders in placental cells are closely associated with adverse pregnancy outcomes, and microRNAs in the placenta play important roles in regulating placental cell behaviors. Placental exosome miRNAs can potentially target maternal cells for intercellular communication between the mother and fetus, serving as novel biomarkers for predicting diseases such as preeclampsia. The transfer of placental miRNAs through exosomes may offer targeted strategies for diagnosing, prognosing, or treating preeclampsia.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Jing Long, Yan Huang, Zhengshan Tang, Yali Shan, Dou Feng, Wenqin Wang, Juan Liu, Ying Huang, Hang Gu, Dewei Guo, Ruojin Yao, Xin Ni
Summary: This study demonstrates that dysfunction of placental 11 beta-hydroxysteroid dehydrogenase type 2 (11β-HSD2) contributes to the development of preeclampsia (PE) by causing mitochondrial dysfunction and mtDNA instability. These abnormalities impair trophoblast function and lead to the development of PE. The study also identifies excess ROS as a potential therapeutic target for treating PE.
Article
Biochemistry & Molecular Biology
Anna Maria Nuzzo, Laura Moretti, Paolo Mele, Tullia Todros, Carola Eva, Alessandro Rolfo
Summary: The conditioned media derived from human placenta-derived mesenchymal stromal cells (hPDMSCs) has shown pro-angiogenic and anti-inflammatory effects on a mouse model of preeclampsia, a severe pregnancy-related syndrome characterized by hypertension, proteinuria, inflammation, and fetal growth restriction. It was found that the hPDMSCs-derived conditioned media could reverse the preeclampsia-like features, including reducing maternal blood pressure, proteinuria, and levels of inflammatory markers.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Immunology
Xiaoqi Wei, Xiuhua Yang
Summary: Preeclampsia (PE) is a unique pregnancy-related disease that can cause maternal and perinatal mortality. Research suggests that natural killer (NK) cells play a central role in immune communication between the fetus and mother, and changes in their count or function may be the cause of PE. This review provides obstetricians with an updated report on the immunological roles of NK cells in PE and suggests that therapeutic measures targeting NK cells are necessary to maintain immune equilibrium.
FRONTIERS IN IMMUNOLOGY
(2023)
Article
Cell Biology
Brooke Grimaldi, Hamid-Reza Kohan-Ghadr, Sascha Drewlo
Summary: Preeclampsia (PE) is a major cause of maternal-fetal morbidity and mortality worldwide. This research shows that placental activation of PPAR gamma can improve the secretion of angiogenic proteins and enhance endothelial function in PE.
Article
Biochemistry & Molecular Biology
Adrian C. Eddy, Chun Yi Chiang, Augustine Rajakumar, Frank T. Spradley, Patricia Dauer, Joey P. Granger, Sarosh Rana
Summary: Preeclampsia is a dangerous complication of pregnancy that can lead to maternal death and long-term complications. This study aimed to find new compounds to reduce placental sFlt-1 and discovered that luteolin showed the most potent inhibition of sFlt-1 release, with over 95% reduction. Luteolin was found to reduce sFlt-1 through inhibition of HIF-1 alpha, possibly via the Akt pathway.
Article
Biochemistry & Molecular Biology
Adrian C. C. Eddy, Chun Yi Chiang, Augustine Rajakumar, Frank T. T. Spradley, Patricia Dauer, Joey P. P. Granger, Sarosh Rana
Summary: Preeclampsia is a serious complication of pregnancy that can lead to maternal death and long-term complications. This study aimed to identify new compounds that can reduce sFlt-1 and inhibit HIF-1a, a prohypertensive factor. The natural compound luteolin showed the strongest inhibition of sFlt-1 release, with over 95% reduction compared to the control group. Luteolin also reduced HIF-1a expression through the Akt pathway. This makes luteolin a potential novel treatment for preeclampsia.
Article
Biochemistry & Molecular Biology
Faith Andres, Natalie J. Hannan, Susan P. Walker, Teresa M. MacDonald, Georgia P. Wong, Ciara Murphy, Ping Cannon, Manju Kandel, Joshua Masci, Tuong-Vi Nguyen, Alison Abboud, Danica Idzes, Valerie Kyritsis, Natasha Pritchard, Stephen Tong, Tuuhevaha J. Kaituu-Lino
Summary: This study found that EPCR levels were significantly increased in both the placenta and circulation of patients with preterm preeclampsia and fetal growth restriction. Hypoxia may be associated with the elevation of placental EPCR. These findings have important implications for understanding the mechanisms underlying these conditions.
Article
Biochemistry & Molecular Biology
Jing Long, Yan Huang, Gang Wang, Zhengshan Tang, Yali Shan, Shiping Shen, Xin Ni
Summary: In this study, it was found that increased maternal glucocorticoid levels were a risk factor for the development of preeclampsia (PE). Pregnant rats exposed to dexamethasone (DEX) exhibited features of PE, impaired spiral artery remodeling, and elevated levels of certain circulatory markers. Abnormal mitochondrial morphology and dysfunction were observed in placentas of DEX rats. The use of a mitochondria-targeted antioxidant alleviated maternal hypertension and renal damage in the DEX-induced PE model. However, scavenging excess ROS did not improve intrauterine growth retardation (IUGR) and elevated levels of certain markers in DEX rats. These findings suggest that excess mitochondrial ROS contributes to trophoblast dysfunction, impaired spiral artery remodeling, reduced uteroplacental blood flow, and maternal hypertension in the DEX-induced PE model, while inflammation and impaired energy metabolism and IGF system may be associated with elevated levels of certain markers and IUGR.
