{"title":"Activin A regulates cellular senescence and decidualization via SMAD3-mediated repression of PPARγ in the endometrium","authors":"Yu Kawaguchi, Kazuya Kusama, Atsuya Tsuru, Mikihiro Yoshie, Junya Kojima, Masanori Ono, Hiritaka Nishi, Kazuhiro Tamura","doi":"10.1016/j.placenta.2026.08.071","DOIUrl":"10.1016/j.placenta.2026.08.071","url":null,"abstract":"","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"183 ","pages":"Page e208"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149199698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
PlacentaPub Date : 2026-09-01Epub Date: 2026-10-16DOI: 10.1016/j.placenta.2026.08.036
Mary Spring, Alys Clark, Jo James
{"title":"Sex-specific differences in placental vascular anatomy in normal and growth-restricted pregnancies","authors":"Mary Spring, Alys Clark, Jo James","doi":"10.1016/j.placenta.2026.08.036","DOIUrl":"10.1016/j.placenta.2026.08.036","url":null,"abstract":"","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"183 ","pages":"Page e197"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149199339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
PlacentaPub Date : 2026-09-01Epub Date: 2026-08-22DOI: 10.1016/j.placenta.2026.08.338
Yan Cao, Li Peng, Yao Chen, Wei Chen
{"title":"Ginkgolide B alleviates placental inflammation and ferroptosis in gestational diabetes through inhibition of the NLRP3 inflammasome and activation of Nrf2/HO-1 signaling","authors":"Yan Cao, Li Peng, Yao Chen, Wei Chen","doi":"10.1016/j.placenta.2026.08.338","DOIUrl":"10.1016/j.placenta.2026.08.338","url":null,"abstract":"<div><h3>Introduction</h3><div>Gestational diabetes mellitus (GDM) occurs in pregnant women of advanced maternal age and is characterized by dysregulated elevation of blood glucose levels. Ginkgolide B (GB) is extracted from <em>Ginkgo biloba</em> leaves and possesses anti-inflammatory as well as antioxidant effects. This study aimed to assess the function of GB in gestational diabetes mellitus (GDM) and explore the underlying mechanisms.</div></div><div><h3>Methods</h3><div>Pregnant C57BL/KsJ-db/+ mice were assigned to the untreated GDM group or treated orally with GB at 100 or 200 mg/kg. Glucose tolerance, insulin sensitivity, fasting blood glucose, plasma insulin levels, and pregnancy outcomes were evaluated. Placental inflammation, oxidative stress, ferroptosis-related proteins, NLRP3 inflammasome components, and proteins involved in the Nrf2/HO-1 signaling pathway were assessed using ELISA, histological staining, immunofluorescence, biochemical assays, and Western blotting.</div></div><div><h3>Results</h3><div>Compared with the Control mice, GDM mice exhibited impaired glucose tolerance and insulin sensitivity, elevated fasting blood glucose and plasma insulin levels, increased placental inflammation and oxidative stress, enhanced ferroptosis, and reduced litter size. GB treatment significantly improved these metabolic and pregnancy-related abnormalities, attenuated inflammatory cytokine production and placental injury, reduced reactive oxygen species accumulation and lipid peroxidation, and restored GPX4 and SLC7A11 expressions. In addition, GB inhibited NLRP3 inflammasome activation, while restoring the expression of Nrf2, HO-1, and NQO1 in placental tissues.</div></div><div><h3>Discussion</h3><div>This study showed the beneficial effects of GB in GDM, suggesting potential therapeutic approaches for preventing the progression of GDM management.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"183 ","pages":"Pages 144-151"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148983580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Placental endoglin protein expression across gestation in normal pregnancy and preeclampsia: Implications for anti-angiogenic therapeutic strategies","authors":"Jayasri Basu, Ashley Armstrong, Liaisan Uzianbaeva, Alireza Mehdizadeh, Magdy Mikhail","doi":"10.1016/j.placenta.2026.09.003","DOIUrl":"10.1016/j.placenta.2026.09.003","url":null,"abstract":"<div><h3>Introduction</h3><div>Preeclampsia is a human-specific hypertensive disorder of pregnancy characterized by new-onset hypertension and proteinuria after 20 weeks of gestation. Placental dysfunction and angiogenic imbalance are central to its pathophysiology. Endoglin, a membrane-bound glycoprotein and precursor of soluble endoglin (sEng), contributes to impaired placentation. This study examined placental endoglin protein expression across normal gestation and compared it with expression in preeclampsia.</div></div><div><h3>Methods</h3><div>Placentas from normotensive pregnancies across all three trimesters and from women with preeclampsia were collected under IRB-approved protocols. Chorionic villi were isolated, and endoglin protein expression was quantified using a monoclonal anti-human Endoglin/CD105 <strong>ELISA</strong> kit, <strong>DY1097</strong>. Of a total of 333 placentas, 324 with gestational age ≥37-weeks comprised the primary dataset, and 9 preeclamptic placentas delivered before 37 weeks were analyzed separately. Group differences were assessed using ANOVA, with significance set at p < 0.05.</div></div><div><h3>Results</h3><div>Endoglin protein expression varied significantly across gestation (p < 0.001). Mean levels (ng/100 mg tissue) were: first trimester 40.94 (n = 116), second trimester 29.24 (n = 79), and third trimester 30.93 (n = 100). Preeclamptic placentas exhibited markedly higher levels (50.77; n = 29). Expression patterns were comparable between Black American and Hispanic women.</div></div><div><h3>Discussion</h3><div>Placental endoglin protein expression peaks in early gestation and is significantly upregulated in preeclampsia. These findings support the role of angiogenic imbalance in disease pathogenesis and provide a biological marker distinguishing normal from pathological placentation. The data also offer a foundation for estimating early pregnancy sEng levels, which may inform dosing strategies for future monoclonal antibody therapies targeting sEng.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"183 ","pages":"Pages 177-185"},"PeriodicalIF":3.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149025851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}