Review: Potential druggable targets for the treatment of early onset preeclampsia

Downing, J. W.; Baysinger, Curtis L.; Johnson, Raymond F.; Paschall, Ray L.

doi:10.1016/j.preghy.2013.04.120

Cited by 7 publications

(4 citation statements)

References 99 publications

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“…Further studies are needed to consolidate the genetic contribution for the lack of response to current or future drugs used in PE, and then pharmacogenomics will likely be considered in treatment of PE. Current efforts in identifying potential new therapeutic targets have been reviewed elsewhere [87][88][89][90]. Next, we review examples of drugs whose responsiveness may be affected by genetic polymorphisms.…”

Section: Potential Novel Drugs For the Treatment Of Pre-eclampsiamentioning

confidence: 99%

Pharmacogenetics in the Treatment of Pre-Eclampsia: Current Findings, Challenges and Perspectives

et al. 2017

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Pre-eclampsia (PE) is defined as pregnancy-induced hypertension and proteinuria, and is a major cause of maternal and perinatal morbidity and mortality. A large subgroup of pregnant women with PE is nonresponsive to antihypertensive drugs, including methyldopa, nifedipine and hydralazine. Pharmacogenomics may help to guide the individualized therapy for this nonresponsive subgroup. However, just a few pharmacogenetic studies examined the effects of genetic polymorphisms on response to antihypertensive drugs in PE, and the criteria of responsiveness used to define responsive or nonresponsive subgroups to antihypertensive therapy should be replicated by others. We review these gene-drugs interactions, novel approaches to pharmacogenomics research and potential novel drugs for PE therapy. Finally, we discuss the challenges and perspectives of pharmacogenetics in the treatment of PE.

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Section: Potential Novel Drugs For the Treatment Of Pre-eclampsiamentioning

confidence: 99%

Pharmacogenetics in the Treatment of Pre-Eclampsia: Current Findings, Challenges and Perspectives

et al. 2017

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“…In a review paper by Downing et al . discussing the potential druggable targets for the treatment of early onset PE, the authors suggested that NO donors are useful for short‐term PE management.…”

Section: Discussionmentioning

confidence: 99%

“…In a review paper by Downing et al 25 discussing the potential druggable targets for the treatment of early onset PE, the authors suggested that NO donors are useful for short-term PE management. In another review paper by Rusin et al, 26 genistein and its derivatives were considered as a NO donor.…”

Section: Discussionmentioning

confidence: 99%

Vascular endothelial growth factor, soluble fms‐like tyrosine kinase 1 and genistein‐induced changes in the vascular reactivity of rat's aorta

Fernandez

Husain

2014

J of Obstet and Gynaecol

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“…Commonly, PE is accompanied by hypertension and proteinuria at or after 20 weeks of pregnancy, providing a potential niche for maternal and infant morbidity and mortality (Li et al, 2020). About 20% of extremely low‐birth‐weight infants who survived suffered from cerebral palsy at 18 months, 10% had visual and/or hearing impairments, and 40% developed disability at 18 years of age (Downing et al, 2013). Abnormal placenta and trophoblast development, poor placental angiogenesis, and increased maternal systemic inflammation are pathophysiologically manifested in PE (Berzan et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA PVT1 accelerates the growth of placental trophoblasts in preeclampsia through the microRNA‐24‐3p/HSD11B2 axis

Wei

Yuan

Yang

2022

Molecular Reproduction Devel

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Long noncoding RNA plasmacytoma variant translocation 1 (PVT1) is essential for the maintenance of normal functions of trophoblasts in preeclampsia (PE). This study aims to decipher the concrete mechanism of PVT1 with the microRNA-24-3p/Type-2 11βhydroxysteroid dehydrogenase (miR-24-3p/HSD11B2) axis in PE. PVT1, miR-24-3p, and HSD11B2 expression levels in normal placental tissues and PE placental tissues were defined. HTR-8/SVneo cells were transfected to determine the effects of PVT1, miR-24-3p, and HSD11B2 on the growth of HTR-8/SVneo cells. The relationships among PVT1/ miR-24-3p/HSD11B2 in HTR-8/SVneo cells were identified. PVT1 and HSD11B2 were downregulated, while miR-24-3p was upregulated in the placenta of PE. Upregulated/ downregulated PVT1 promoted/impeded the growth of human placental trophoblast (HTR-8/SVneo) cells in PE. Restored/knocked down miR-24-3p impeded/enhanced the growth of HTR-8/SVneo cells in PE. PVT1 inhibited miR-24-3p to mediate HSD11B2.

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Review: Potential druggable targets for the treatment of early onset preeclampsia

Cited by 7 publications

References 99 publications

Pharmacogenetics in the Treatment of Pre-Eclampsia: Current Findings, Challenges and Perspectives

Pharmacogenetics in the Treatment of Pre-Eclampsia: Current Findings, Challenges and Perspectives

Vascular endothelial growth factor, soluble fms‐like tyrosine kinase 1 and genistein‐induced changes in the vascular reactivity of rat's aorta

Long noncoding RNA PVT1 accelerates the growth of placental trophoblasts in preeclampsia through the microRNA‐24‐3p/HSD11B2 axis

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