Placenta最新文献

{"title":"Macrophage at maternal-fetal Interface: Perspective on pregnancy and related disorders.","authors":"Haoran Duan, Weinan Deng, Julia Kzhyshkowska, Dunjin Chen, Shuang Zhang","doi":"10.1016/j.placenta.2025.05.005","DOIUrl":"https://doi.org/10.1016/j.placenta.2025.05.005","url":null,"abstract":"<p><p>Immune cells at the maternal-fetal interface (MFI) undergo dynamic changes to facilitate fetal growth and development during pregnancy. In contrast to the adaptive immune system, where effector T cells, Tregs, and suppressor T cells play key roles in maintaining immune tolerance toward the semi-allogeneic fetus, the innate immune system-comprising decidual nature killer (dNK) cells, macrophages, and dendritic cells (DCs)-makes up a significant portion of the decidual leukocyte population. These innate immune cells are crucial in modulating trophoblast invasion, spiral artery remodeling, and apoptotic cell phagocytosis. Dysregulation of the innate immune system has been linked to impaired uterine vessel remodeling and defective trophoblast invasion, which can lead to complications such as spontaneous abortion, preeclampsia (PE), and preterm. This review focuses on recent advancements in understanding the innate immune defenses at the maternal-fetal interface and their connections to pregnancy-related diseases, with particular emphasis on the role of macrophages.</p>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144120656","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":"Recent advances in multimodal approaches for investigating placental development and related diseases.","authors":"Hao Wang, Tao Zhang, Jing Ruan, Xi Zheng, Shuwei Zheng, Qiqi Liu, Fen He, Bo Sun, Qi Zhang, Yuanfang Zhu, Xiaoyan Chen","doi":"10.1016/j.placenta.2025.05.004","DOIUrl":"https://doi.org/10.1016/j.placenta.2025.05.004","url":null,"abstract":"<p><p>The placenta is a vital organ that supports fetal growth and pregnancy maintenance. Its dysfunction is associated with severe complications, including preeclampsia, fetal growth restriction, and placenta accreta spectrum disorders. Traditional approaches to placental research have provided valuable insights but are limited in capturing the complexity of this dynamic organ. In recent years, multimodal approaches-integrating advanced imaging, single-cell and spatial omics, and artificial intelligence (AI)-have enabled comprehensive analyses of placental development and disease. These strategies offer improved diagnostic accuracy, deeper molecular understanding, and real-time assessment of placental function. This review summarizes recent advances in multimodal placental research, highlighting key technologies such as ultrasound and MRI, single-cell transcriptomics, spatial profiling, and AI-based prediction models. Particular emphasis is placed on contributions from Chinese research teams, who have developed novel platforms, atlases, and clinically relevant tools. We also discuss ongoing challenges, including data standardization, interpretability of AI models, and ethical considerations. Looking ahead, the integration of multimodal data with AI and wearable technologies holds promise for precision obstetrics and individualized pregnancy care. Together, these innovations are advancing both scientific understanding and clinical management of placenta-related disorders.</p>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079868","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":"Cytotoxicity and induction of proinflammatory cytokines in placental explant cells following azathioprine exposure.","authors":"Franciele Rodrigues Araújo, Adriana Lopes da Silva, Leandro de Oliveira, Simone Correa-Silva, Estela Bevilacqua","doi":"10.1016/j.placenta.2025.05.002","DOIUrl":"https://doi.org/10.1016/j.placenta.2025.05.002","url":null,"abstract":"<p><p>Immunosuppressive drugs offer hope for the survival and motherhood of women with various disorders. Although the systemic side effects of these drugs on mothers have been studied, their impact on the placenta remains poorly understood, which can negatively affect fetal and postnatal development. This study investigated the effects of Azathioprine, an immunosuppressive drug, on the chorionic villi of human placentas from healthy pregnancies, focusing on cellular vitality and pro-inflammatory cytokines expression. Chorionic villi from term placentas were cultured and treated with Azathioprine at concentrations ranging from 0 to 100 ng/mL for 24 h. Azathioprine reduced mitochondrial metabolic activity (MTT assay) at all concentrations tested (p < 0.05) and increased cellular injury rates (LDH assay) at 50 and 100 ng/mL (p < 0.05). It also elevated protein (at 12.5 and 25 ng/mL, p < 0.05) and gene expression levels of interleukin (IL)-1β (12.5 ng/mL, p < 0.05). Protein levels of IL-18 increased significantly following Azathioprine exposure (p < 0.05), along with cleaved Caspase-1 (p = 0.003) and phosphorylated NF-κB levels (p < 0.05), compared to controls. IL-18 gene expression was elevated only at 12.5 ng/mL (p < 0.0005). These findings suggest that Azathioprine creates a cytotoxic microenvironment that disrupts the metabolism of chorionic villi, leading to injury and activation of pro-inflammatory cytokine expression. Such changes may contribute to an imbalance in placental homeostasis, potentially associated with adverse maternal and neonatal outcomes that warrant further investigation.</p>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143394","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":"Relationship between fetal inflammatory response syndrome and stages of acute placental inflammation stratified by the presence or absence of preterm premature rupture of membranes","authors":"Keisuke Tsumura ,&nbsp;Fumio Yamasaki ,&nbsp;Makoto Nomiyama ,&nbsp;Kae Yamaguchi ,&nbsp;Aisa Sugimoto ,&nbsp;Mika Obata ,&nbsp;Takashi Shimomura ,&nbsp;Yousuke Oka ,&nbsp;Yuko Oshima ,&nbsp;Takeshi Ono ,&nbsp;Mitsuyo Noguchi ,&nbsp;Yutaka Kozuma ,&nbsp;Yukiko Nakura ,&nbsp;Itaru Yanagihara ,&nbsp;Masatoshi Yokoyama","doi":"10.1016/j.placenta.2025.05.001","DOIUrl":"10.1016/j.placenta.2025.05.001","url":null,"abstract":"<div><h3>Introduction</h3><div>Fetal inflammatory response syndrome (FIRS) is a critical condition associated with increased neonatal morbidity and mortality, regardless of gestational age at birth. This study aimed to determine the frequency of FIRS at each stage of acute placental inflammation, stratified by the presence or absence of preterm premature rupture of membranes (PPROM).</div></div><div><h3>Methods</h3><div>This study included singleton pregnant women with spontaneous preterm births. Fetal inflammatory response syndrome was defined as an umbilical cord vein interleukin-6 concentration of &gt;11.0 pg/mL. Stages of acute placental inflammation were categorized into maternal inflammatory response (MIR) and fetal inflammatory response (FIR), as defined by the Amsterdam Placental Workshop Group Consensus Statement.</div></div><div><h3>Results</h3><div>In total, 584 pregnant women (300 with PPROM and 284 without PPROM) met the inclusion criteria. Predictive ability of the MIR stage for FIRS was higher than that of the FIR stage, with area under the receiver operating characteristic curve values of 0.85 and 0.80, respectively (P = 0.05). Frequencies of FIRS in patients with PPROM were 5 %, 64 %, 75 %, and 71 % for no MIR and MIR stages 1, 2, and 3, respectively; in patients without PPROM, the frequencies were 7 %, 26 %, 40 %, and 81 %, respectively. The frequency of FIRS was significantly higher in patients with PPROM than that in those without PPROM at MIR stages 1 and 2 (18/28 vs. 6/23, P = 0.01; 18/24 vs. 6/15, P = 0.04).</div></div><div><h3>Discussion</h3><div>These results demonstrate the importance of considering both MIR stage and the presence or absence of PPROM when predicting FIRS based on placental pathology.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"167 ","pages":"Pages 64-70"},"PeriodicalIF":3.0,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143905862","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":"Corrigendum to “Platelet alloimmunization is associated with low grade chronic histiocytic intervillositis - A new link to a rare placental lesion?” [Placenta 112 (2021) 89–96]","authors":"Nora Hersoug Nedberg ,&nbsp;Gitta Turowski ,&nbsp;Katarzyna Guz ,&nbsp;Ewa Przytuła ,&nbsp;Małgorzata Uhrynowska ,&nbsp;Borghild Roald ,&nbsp;Anne Husebekk ,&nbsp;Vasilis Sitras ,&nbsp;Mona Nystad ,&nbsp;Marzena Dębska ,&nbsp;Ewa Brojer ,&nbsp;Heidi Tiller","doi":"10.1016/j.placenta.2025.04.030","DOIUrl":"10.1016/j.placenta.2025.04.030","url":null,"abstract":"","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"167 ","pages":"Page 63"},"PeriodicalIF":3.0,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143905863","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":"The POHaD paradigm: role of the placenta in paternal programming.","authors":"Evangelina Capobianco, Irune Pirrone","doi":"10.1016/j.placenta.2025.04.027","DOIUrl":"https://doi.org/10.1016/j.placenta.2025.04.027","url":null,"abstract":"<p><p>The Paternal Origins of Health and Disease (POHaD) paradigm emerges from the well-known Developmental Origins of Health and Disease (DOHaD) concept. Research into the programming of metabolic diseases originating from the paternal germline began over 20 years ago, focusing on the father's pre-conceptional exposure, such as metabolic disorders and lifestyle habits (kind of diet, exercise, smoking, drugs consumption, etc.). This exposure can lead to epigenetic marks not only in his germ cells but also in other components of the semen that impact the health of future generations. The significant role of the paternal genome in the fetal component of the placenta and the recognition of the placenta's involvement in postnatal disease programming underscore the importance of studying the placenta in paternal programming research. The aim of this work is to review what we know so far about paternal programming highlighting the variations in the phenotype of the placenta and the influence of it in the programming of metabolic pathologies in the offspring of fathers exposed to metabolic disorders such as obesity and diabetes.</p>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144064544","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":"The roles of maternal one-carbon metabolism and placental imprinted gene expression in placental development and somatic growth in a longitudinal birth cohort","authors":"Olivia R. Gutherz ,&nbsp;Qian Li ,&nbsp;Maya Deyssenroth ,&nbsp;Helen Wainwright ,&nbsp;Joseph L. Jacobson ,&nbsp;Ernesta M. Meintjes ,&nbsp;Jia Chen ,&nbsp;Sandra W. Jacobson ,&nbsp;R. Colin Carter","doi":"10.1016/j.placenta.2025.04.017","DOIUrl":"10.1016/j.placenta.2025.04.017","url":null,"abstract":"<div><h3>Objectives</h3><div>One-carbon nutrients and imprinted genes both play critical roles in placental development and somatic growth. We aimed to examine (1) the impact of maternal one-carbon nutrition on placental imprinted gene expression, placental development, and infant growth and (2) interactions between one-carbon nutrients and imprinted genes in placental development and infant growth.</div></div><div><h3>Methods</h3><div>Women were interviewed prenatally about demographics and their alcohol, smoking, and drug use during pregnancy in a prospective longitudinal cohort study examining developmental effects of prenatal alcohol exposure in Cape Town, South Africa (<em>N</em> = 158). Erythrocyte folate, serum vitamin B12, and plasma choline concentrations were assayed at recruitment. Infant weight and height were assessed at age 2 weeks. Placental histopathology exams and placental expression of 109 imprinted genes (Nanostring) were assessed (<em>n</em> = 65).</div></div><div><h3>Results</h3><div>In limma tests, women with plasma choline concentrations below the median had lower placental expression of <em>EPS15</em>, <em>IGF2R</em>, <em>LINC00657</em>, <em>SGCE</em>, <em>ZC3H12C</em>, and <em>ZNF264</em> than women above the median (<em>p</em> &lt; 0.05, FDR&lt;0.10). In regression models adjusted for potential confounders, plasma choline (μM) was associated with larger placental weight (g) (B = 14.0(1.9, 26.2)) and reduced maternal vascular underperfusion (MVU) prevalence (B = −0.07(-0.12, −0.02). Trends were seen for mediation of the relation between choline and MVU by decreased <em>LINC00657</em>, <em>ZC3H12C</em>, and <em>ZNF264</em> expression. In regression models examining plasma cholineXimprinted gene expression interaction effects, plasma choline modified relations of <em>EPS15</em>, <em>ZC3H12C,</em> and <em>ZNF264</em> to placental weight and fetal growth.</div></div><div><h3>Conclusions</h3><div>These findings suggest maternal choline status may impact placental and fetal development, with imprinted genes playing potential mechanistic roles.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"167 ","pages":"Pages 109-121"},"PeriodicalIF":3.0,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143937507","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":"Dymanics of stroke in pregnant women with preeclampsia","authors":"Gulfairuz Urazbayeva ,&nbsp;Almagul Kurmanova ,&nbsp;Aigul Terlikbayeva ,&nbsp;Laura Kayupova ,&nbsp;Damilya Salimbaeva","doi":"10.1016/j.placenta.2025.04.029","DOIUrl":"10.1016/j.placenta.2025.04.029","url":null,"abstract":"<div><h3>Introduction</h3><div>Preeclampsia is one of the leading causes of maternal mortality in Kazakhstan, with its prevalence rising in recent years. The condition poses significant risks to both maternal and neonatal health. Identifying prognostic criteria for stroke development among women with preeclampsia is essential for improving outcomes<strong>. Methods.</strong> This study evaluated the diagnostic significance of clinical features and risk factors for stroke in pregnant women with preeclampsia. A retrospective analysis was conducted on 200 pregnant women divided into two groups: 100 women with acute cerebrovascular events associated with preeclampsia (main group) and 100 women with preeclampsia but without stroke (comparison group). Data were collected from 2016 to 2022, focusing on clinical, anamnestic, and laboratory markers. <strong>Results</strong>. Significant differences in risk factors were observed between the two groups. Key predictors of stroke in the context of preeclampsia included advanced maternal age (&gt;35 years), obesity, a maternal family history of stroke, and a history of stillbirth. Adverse outcomes such as emergency caesarean sections, maternal death, intrauterine foetal death, and early neonatal death were more frequent in the main group compared to the comparison group. <strong>Discussion</strong>. The findings highlight the need for early identification and monitoring of high-risk pregnancies to prevent stroke and improve maternal and neonatal outcomes. Proactive interventions based on these risk factors can help mitigate maternal and perinatal morbidity and mortality in Kazakhstan.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"167 ","pages":"Pages 80-86"},"PeriodicalIF":3.0,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143911403","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":"Fibroblast growth factor 7 facilitates invasion of human trophoblast cells through the JNK pathway during pregnancy","authors":"Lijuan Li ,&nbsp;Yu Zhou ,&nbsp;Wenjie Zhou ,&nbsp;Yang Liu ,&nbsp;Jie Mei","doi":"10.1016/j.placenta.2025.04.025","DOIUrl":"10.1016/j.placenta.2025.04.025","url":null,"abstract":"<div><h3>Introduction</h3><div>This study investigates the role of FGF7 in trophoblast invasion under high estrogen and progesterone levels, focusing on the JNK signaling pathway. The aim is to demonstrate that FGF7 enhances human trophoblast cell invasion via JNK activation, crucial for establishing pregnancy.</div></div><div><h3>Methods</h3><div>We investigated the expression of FGF7 in primary human trophoblasts to evaluate the effects of elevated estrogen and progesterone levels on trophoblast invasion. The study focused on the role of FGF7 in gestational regulation and its mechanism of activating the JNK signaling pathway through FGFR2.</div></div><div><h3>Results</h3><div>The study unveiled that FGF7 and FGFR2 are expressed in trophoblast cells during normal pregnancies, with the expression of FGF7 being upregulated by estrogen and progesterone. In trophoblastic cells, FGF7 activates the MAPK/JNK signaling pathway, resulting in upregulation of MMP-2 and MMP-9 expression, concomitant downregulation of TIMP-1 and TIMP-2 expression, and ultimately enhanced invasive capacity. However, in cases of recurrent spontaneous abortion (RSA), the levels of FGF7/FGFR2 expression exhibited a notable decrease. These results indicate that the involvement of FGF7/FGFR2 could be significant in maintaining normal pregnancy by regulating trophoblast invasiveness, and their impaired expression could contribute to RSA.</div></div><div><h3>Discussion</h3><div>The present study elucidates the role of FGF7 in facilitating trophoblast invasion through activation of the MAPK/JNK pathway and upregulation of MMPs, thereby providing potential therapeutic insights for recurrent spontaneous abortion (RSA) attributed to impaired trophoblast invasion.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"167 ","pages":"Pages 87-94"},"PeriodicalIF":3.0,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143921897","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":"Single-cell RNA sequencing reveals altered placental microenvironment due to maternal high-fat diet","authors":"Xing-yu Lu ,&nbsp;Yi-dan Xu ,&nbsp;Qian-ren Zhang ,&nbsp;Yi-nan Jiang ,&nbsp;Hai-nan Chen ,&nbsp;Ping Ji ,&nbsp;Ying Wang ,&nbsp;Wei-hong Zeng ,&nbsp;Yan Dong","doi":"10.1016/j.placenta.2025.04.011","DOIUrl":"10.1016/j.placenta.2025.04.011","url":null,"abstract":"<div><h3>Background</h3><div>The prevalence of childhood metabolic diseases has markedly increased in recent decades whereas the effects of maternal nutrients affecting the placental microenvironment are not clearly addressed.</div></div><div><h3>Methods</h3><div>In the present study, female C57BL/6J mice were fed with a high-fat diet (HFD) or control diet (CON) for 5 weeks prior to mating and then during pregnancy. Single-cell RNA sequencing (scRNA-seq) was used to dissect the placental cell atlas at embryonic day(E) 18.5<strong>.</strong></div></div><div><h3>Results</h3><div>Maternal HFD led to a reduction in the composition of placental labyrinth zone (LZ) trophoblast cells and endothelial cells, together with a diminished LZ area and narrowed fetal vessels, related to a decreased placental efficiency. Pro-inflammatory placental NK1 cells and M1-like macrophages were more apparent in the placenta from HFD dams with inflammation features. Increased glycogen deposition and glycogen trophoblast cells were also detectable in the HFD placenta, likely associated with the altered metabolism of placental NK cells and macrophages.</div></div><div><h3>Conclusions</h3><div>Maternal HFD before and during pregnancy leads to an altered placental microenvironment with more inflammatory features and abnormal metabolic properties, which provides a better understanding on the mechanisms of intergenerational inheritance.</div></div>","PeriodicalId":20203,"journal":{"name":"Placenta","volume":"167 ","pages":"Pages 140-151"},"PeriodicalIF":3.0,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144068653","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}