Jordan H Mallette, Breland F Crudup, Barbara T Alexander
{"title":"子痫前期的生长限制:来自动物模型的教训","authors":"Jordan H Mallette, Breland F Crudup, Barbara T Alexander","doi":"10.1016/j.cophys.2023.100647","DOIUrl":null,"url":null,"abstract":"<div><p>Preeclampsia remains a major health concern for mother and child. Yet, treatment options remain limited to early delivery. Placental dysfunction in preeclampsia occurs in response to an increase in oxidative stress<span><span> and inflammatory cytokines with vasoactive and antiangiogenic factors contributing to impaired maternal and fetal health. Moreover, recent studies indicate a potential role for epigenetic mediators in the pathophysiology of placental ischemia. Numerous </span>animal models<span><span> are utilized to explore the pathogenesis of preeclampsia and fetal growth restriction. This review provides a brief overview of recent progress in </span>preclinical studies regarding potential therapeutic targets for the treatment and prevention of preeclampsia with an emphasis on fetal growth restriction and the fetal programming of increased cardiovascular risk.</span></span></p></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"32 ","pages":"Article 100647"},"PeriodicalIF":2.5000,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10035651/pdf/","citationCount":"1","resultStr":"{\"title\":\"Growth restriction in preeclampsia: lessons from animal models\",\"authors\":\"Jordan H Mallette, Breland F Crudup, Barbara T Alexander\",\"doi\":\"10.1016/j.cophys.2023.100647\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Preeclampsia remains a major health concern for mother and child. Yet, treatment options remain limited to early delivery. Placental dysfunction in preeclampsia occurs in response to an increase in oxidative stress<span><span> and inflammatory cytokines with vasoactive and antiangiogenic factors contributing to impaired maternal and fetal health. Moreover, recent studies indicate a potential role for epigenetic mediators in the pathophysiology of placental ischemia. Numerous </span>animal models<span><span> are utilized to explore the pathogenesis of preeclampsia and fetal growth restriction. This review provides a brief overview of recent progress in </span>preclinical studies regarding potential therapeutic targets for the treatment and prevention of preeclampsia with an emphasis on fetal growth restriction and the fetal programming of increased cardiovascular risk.</span></span></p></div>\",\"PeriodicalId\":52156,\"journal\":{\"name\":\"Current Opinion in Physiology\",\"volume\":\"32 \",\"pages\":\"Article 100647\"},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2023-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10035651/pdf/\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Current Opinion in Physiology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2468867323000172\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"PHYSIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Opinion in Physiology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2468867323000172","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
Growth restriction in preeclampsia: lessons from animal models
Preeclampsia remains a major health concern for mother and child. Yet, treatment options remain limited to early delivery. Placental dysfunction in preeclampsia occurs in response to an increase in oxidative stress and inflammatory cytokines with vasoactive and antiangiogenic factors contributing to impaired maternal and fetal health. Moreover, recent studies indicate a potential role for epigenetic mediators in the pathophysiology of placental ischemia. Numerous animal models are utilized to explore the pathogenesis of preeclampsia and fetal growth restriction. This review provides a brief overview of recent progress in preclinical studies regarding potential therapeutic targets for the treatment and prevention of preeclampsia with an emphasis on fetal growth restriction and the fetal programming of increased cardiovascular risk.