bims-placeb Biomed News
on Placental cell biology
Issue of 2026–10–25
fourteen papers selected by
Carlos M Guardia, National Institute of Environmental Health Sciences
  1. Proteomic Profiling of Xenobiotic and Nutrient Transporters in Human Placenta of Different Gestational Ages.
  2. Lineage-specific and gestational age-dependent DNA methylation programming orchestrates human placental development.
  3. XIST drives X-chromosome inactivation and safeguards female extraembryonic cells in humans.
  4. Loss of KAT5-dependent H2A.Z acetylation provokes chromosomal instability in recurrent pregnancy loss.
  5. Hypoxia-Driven CA2 Promotes Trophoblast Dysfunction in Preeclampsia.
  6. FUBP1 lactylation suppresses trophoblast function in fetal growth restriction.
  7. Trophoblast-derived extracellular vesicles elicit long-term effects on maternal cardiovascular function in a postpartum model of chronic hypertension.
  8. Placental mitochondrial impairment in preeclampsia patients.
  9. First Transcriptomic Insights into the Invertebrate Placental Analogue: Differential Gene Expression in Gonozooids of Crisiella producta (Bryozoa, Cyclostomatida).
  10. Ellagic acid alleviates nicotine-induced placental injury in pregnant rats: Histomorphometric and molecular evidence.
  11. Placental adaptation to maternal overnutrition as an evolutionary trade-off.
  12. Maternal diet and placental outcomes: Evidence of sexual dimorphism among mothers with overweight and obesity.
  13. Multiplexed embryo profiling links cellular state to zygotic genome activation in single cells.
  14. Exercise in pregnant elite athletes: Physiological considerations, risks, and benefits.
  1. Clin Pharmacol Ther. 2026 Oct 20.
    Proteomic Profiling of Xenobiotic and Nutrient Transporters in Human Placenta of Different Gestational Ages.
    Eric M Weaver, Ariel Topletz-Erickson, Edward J Kelly, Joanne Wang, Nina Isoherranen, Jashvant D Unadkat, Samuel L M Arnold.
      The placenta serves a critical role in nutrient uptake and waste elimination for the developing fetus. The placenta is also responsible for the uptake and/or exchange of xenobiotics, including medications, between the maternal and fetal bloodstreams. An estimated 40-80% of women take medications or drugs during pregnancy. Very little is understood about fetal drug and nutrient exposure during pregnancy and how it may change over the course of fetal development. This study aimed to characterize the abundance of transport proteins in placental tissue, which are important in modulating fetal nutrient and drug exposure, over the duration of pregnancy. Using a mass spectrometry-based global proteomic approach, the relative abundance of proteins in placental tissue samples was profiled from first trimester, second trimester, and term placenta samples. Our analysis detected a total of 6331 proteins which included a total of 139 solute carrier and ATP-binding cassette transport proteins that were detected across the dataset, and 80 that were quantified in every sample. In general, membrane-associated proteins, including solute carrier and ATP-binding cassette transport proteins, were significantly enriched in placental tissue collected during early gestation compared to term placental tissue. Overall, this study presents a comprehensive profiling of membrane-associated proteomic changes during gestation and identifies significant gestational age associated abundance changes at the protein level in several transport protein families. These data provide critical information to support future studies into the understanding of fetal exposure to xenobiotics and nutrients circulating in the maternal bloodstream.
    DOI:  https://doi.org/10.1002/cpt.70525
  2. Sci Adv. 2026 Oct 23. 12(43): eaee0560
    Lineage-specific and gestational age-dependent DNA methylation programming orchestrates human placental development.
    Shanru Yi, Jing Xiao, Ruixue Wang, Mengting Wang, Chunyan Le, Guang Yang, Shanshan Yi, Wenju Liu, Hong Wang, Xiaocui Li, Xiaoyu Liu, Kai Wang, Cizhong Jiang, Shaorong Gao, Jiayu Chen.
      The human placenta is essential for pregnancy, yet the dynamic regulation of its DNA methylome during development remains poorly understood. To address this, we generated a single base-resolution DNA methylation atlas of human placental trophoblasts across gestation. We identified a lineage-specific methylation program established immediately after implantation, followed by gestational age-dependent methylation accumulation. This program acted as a developmental barrier that coordinated placental maturation and immune homeostasis. By integrating histone modifications and functional perturbations, we revealed a temporal dynamic between H3K27me3 and DNA methylation that silenced proinflammatory loci and a switch from H3K9me3 to DNA methylation at repeat elements to maintain genome stability. Aberrant methylation in preterm placentas underscored the physiological importance of methylation regulation. Using human trophoblast stem cells, we demonstrated that DNMT1 was critically required for maintaining trophoblast methylome integrity and self-renewal, while the DNMT3 family were equally essential for trophoblast survival. Overall, we established a placenta-specific epigenetic framework for human trophoblast development.
    DOI:  https://doi.org/10.1126/sciadv.aee0560
  3. Nat Commun. 2026 Oct 22. pii: 10738. [Epub ahead of print]17(1):
    XIST drives X-chromosome inactivation and safeguards female extraembryonic cells in humans.
    Amitesh Panda, Léo Carrillo, Bradley Philip Balaton, Jeanne Brouillet, Solomon Nshemereirwe, Jarne Bonroy, Charbel Alfeghaly, Romina Facchinello, Sherif Khodeer, Nicolas Peredo, Ruben Boers, Gael Castel, Charlie London, Emmanuel Cazottes, Madeleine Moscatelli, Raissa Songwa Tchinda, Thi Xuan Ai Pham, San Kit To, Ryan Nicolaas Allsop, Yang Wang, Desislava Staneva, Peter J Rugg-Gunn, Kathy K Niakan, Joost Gribnau, Jean-François Ouimette, Claire Rougeulle, Vincent Pasque.
      X-chromosome inactivation (XCI) is essential for extraembryonic tissue growth and embryo development in mice. However, species-specific differences in its timing and regulation have left its role in human development unclear. Here, we show that the in vitro differentiation of naive human pluripotent stem cells to trophoblast stem cells and extraembryonic mesoderm cells is accompanied by XCI. The inactive X chromosome displays an atypical chromatin state, lacking DNA methylation and canonical heterochromatin marks. We demonstrate that extraembryonic differentiation and XCI are temporally linked. Using loss of function approaches, we found that XIST is required for XCI establishment in humans. Furthermore, we show that XCI is needed for the survival of human female extraembryonic cells. Together, these findings link XCI to the formation of human extraembryonic lineages, with important implications for human reproductive biology.
    DOI:  https://doi.org/10.1038/s41467-026-78394-z
  4. Sci Adv. 2026 Oct 23. 12(43): eaef6029
    Loss of KAT5-dependent H2A.Z acetylation provokes chromosomal instability in recurrent pregnancy loss.
    Shilei Bi, Yongjie Chen, Lizi Zhang, Jiahui Zhang, Yijing Wang, Baoying Huang, Shanze Li, Lijun Huang, Yifan Wang, Huarong Wang, Ranran Meng, Zhaowei Tu, Lili Du, Haibin Wang, Zhijian Wang, Dunjin Chen, Shuang Zhang, Fengchao Wang.
      Placenta defects are one of the major causes of miscarriages, yet the underlying mechanisms remain poorly understood. We demonstrate that trophoblast-specific depletion of the acetyltransferase Kat5, or introduction of acetylation-defective mutants Kat5-Q377E G380E and Kat5-Y47A, induces severe chromosomal instability (CIN) during trophoblast cells division, leading to embryonic lethality. Moreover, mutation of a key lysine acetyltransferase 5 (KAT5) substrate, H2A.Z, via the introduction of H2az1-K5R K8R K12R K14R (which prevents H2A.Z acetylation), phenocopies the effects of KAT5 loss. Integrated RNA sequencing and CUT&Tag in mouse trophoblast stem cells reveal that KAT5, through H2A.Z acetylation, regulates transcription of key mitotic genes (Aurka, Aurkb, and Cenpa). We extend our finding to human trophoblast stem cells, demonstrating a conserved role for KAT5 in preventing CIN. Clinical analysis of placental villi from recurrent pregnancy loss patients with copy number variations revealed reduced expression of KAT5 and acetylated H2A.Z. This study demonstrates that the conserved KAT5-H2A.Z acetylation pathway safeguards chromosomal stability in trophoblast cells, supporting placenta development and successful pregnancy.
    DOI:  https://doi.org/10.1126/sciadv.aef6029
  5. FASEB J. 2026 Oct 31. pii: e72381. [Epub ahead of print]40(20):
    Hypoxia-Driven CA2 Promotes Trophoblast Dysfunction in Preeclampsia.
    Lujiao Chen, Chuchu Zhu, Jian Zhao, Lei Ye, Hetong Li, Haote Han, Ying Jiang, Qiong Luo.
      Explore the potential function of Carbonic Anhydrase 2 (CA2) in the pathophysiology of preeclampsia. Peripheral blood and placental samples were collected from healthy pregnant women and patients with preeclampsia. Placental CA2 expression was validated in independent clinical cohorts and experimental mouse models. HTR-8/SVneo cells were cultured and transfected with a CA2 overexpression plasmid to evaluate trophoblast dysfunction. Bulk RNA sequencing was performed to identify downstream genes associated with CA2 overexpression, followed by VEGFA rescue experiments. Hypoxia-related regulation of CA2 was investigated. Lipid nanoparticle (LNP)-encapsulated siRNA against CA2 was constructed in an L-NAME-induced PE model to evaluate therapeutic effects. CA2 expression was significantly increased in placental tissues and maternal serum from women with PE and was also elevated in experimental PE mouse models. CA2 predominantly localized in trophoblast cells, and correlated positively with serum creatinine and urea and correlated negatively with fetal birth weight. CA2 overexpression markedly suppressed trophoblast proliferation, migration, and invasion, without affecting apoptosis. Transcriptomic analysis suggested that vascular endothelial growth factor A (VEGFA) acted as a downstream mediator of CA2, and VEGFA overexpression partially rescued CA2-induced trophoblast dysfunction. CA2 expression was upregulated under hypoxic conditions and regulated by hypoxia-inducible factor-1α (HIF-1α). LNP-mediated CA2 silencing partially improved placental structure and fetal outcomes in vivo. CA2 is upregulated in the preeclamptic placenta and is associated with placental dysfunction and adverse fetal outcomes. Mechanistically, CA2 may act downstream of HIF-1α and contribute to trophoblast dysfunction partly through modulation of VEGFA signaling, and CA2 silencing partially improved maternal and fetal outcomes, highlighting CA2 as a potential therapeutic target for preeclampsia.
    Keywords:  CA2; HIF‐1α; VEGFA; preeclampsia; trophoblast cells
    DOI:  https://doi.org/10.1096/fj.202602024R
  6. Clin Epigenetics. 2026 Jul 23. pii: 188. [Epub ahead of print]18(1):
    FUBP1 lactylation suppresses trophoblast function in fetal growth restriction.
    Xinyue Liang, Shenshen Yao, Jian Ma, Dan Wang.
       BACKGROUND: Fetal growth restriction (FGR) is a common complication of pregnancy; however, its exact molecular mechanisms remain unclear. Excessive lactate accumulation in the placenta is often observed during FGR. High concentrations of lactate can regulate the proliferation of pathological cells through lactylation of key proteins. Therefore, we aimed to screen key lactylation modification-related genes (LMRGs) and provide new directions for the diagnosis and treatment of FGR.
    METHODS: The Differentially expressed LMRGs (DE-LMRGs) in FGR were evaluated using the Gene Expression Omnibus database. Functional enrichment analysis was performed, and a protein-protein interaction (PPI) network was created to explore the characteristics of placental gene networks associated with FGR. In addition, secondary cluster analysis was performed using a machine learning algorithm to screen critical genes. We evaluated the degree of immune cell infiltration of key genes using single-sample gene set enrichment analysis. The expression and function of key genes in FGR were verified experimentally. Furthermore, FUBP1 lactylation was assessed using mass spectrometry and immunoprecipitation. We overexpressed wild-type and mutant FUBP1 in HTR-8/SVneo cells to investigate how its lactylation regulates trophoblast function. Finally, patient-derived organoids (PDO) were cultured to confirm the underlying mechanism of FUBP1.
    RESULTS: In total, 35 DE-LMRGs were identified, and their PPI network was constructed. Two distinct FGR clusters were obtained using unsupervised consensus clustering. Moreover, the DE-LMRGs between the two patterns were mainly enriched in immune cell regulation-related molecular functions. We identified 5 overlapping key genes (BCLAF1, FUBP1, S100A6, CSRP1, CSRP2) by integrating the LASSO, random forest (RF), and SVM-RFE algorithms and screening for genes with a large fold change (using log2-FC). FUBP1 and BCLAF1 expression was lower in FGR placental tissues than in normal controls. Functional assays showed that both genes typically promote HTR-8/SVneo cell proliferation and invasion. However, lactylation of FUBP1 exerted the opposite effect by inhibiting proliferation and invasion and promoting apoptosis, indicating that FUBP1 lactylation regulates trophoblast function. Furthermore, PDO derived from the trophoblast tissues of patients with FGR revealed that FUBP1 lactylation suppressed PDO formation.
    CONCLUSIONS: FUBP1 lactylation is identified as a novel mechanism suppressing trophoblast function in FGR. This finding expands the field of FGR research by highlighting the role of lactylation-modified proteins and provides crucial insights into the pathological mechanisms of FGR.
    Keywords:  BCLAF1; FUBP1; Fetal growth restriction; Lactylation; Organoids
    DOI:  https://doi.org/10.1186/s13148-026-02208-8
  7. Am J Physiol Heart Circ Physiol. 2026 Nov 01. 331(5): H1795-H1811
    Trophoblast-derived extracellular vesicles elicit long-term effects on maternal cardiovascular function in a postpartum model of chronic hypertension.
    Sophie Piesse, Sien Yee Lau, Yang Liu, Charlotte Oyston, Katie Groom, Qi Chen, Larry Chamley, Carolyn J Barrett.
      The hypertensive disease of pregnancy, preeclampsia, is a risk factor for future maternal cardiovascular disease while normal pregnancy is cardioprotective in the long term. Trophoblast-derived extracellular vesicles (T-EVs) released by the placenta are implicated in the development of vascular dysfunction and are widely thought to have a role in the pathogenesis of preeclampsia. This study tested the effects of T-EVs from both normotensive and preeclamptic pregnancies on long-term cardiovascular outcomes in a pregnant hypertensive model. Spontaneously hypertensive rats (SHRs) received intravenous vehicle control (CTEV; n = 11), and T-EVs from normotensive (NT; n = 10), early onset preeclamptic (EOPE; n = 10), or late-onset preeclamptic (LOPE; n = 10) pregnancies between days 8.5 and 18.5 of pregnancy (term = 22.5 days). SHRs were monitored during pregnancy and up to 12 mo postpartum, with noninvasive blood pressure plethysmography and echocardiography, followed by wire myography and histology. The NT group demonstrated significantly lower postpartum systolic blood pressure (SBP) compared with CTEV (P < 0.0001), whereas SBP in the EOPE group was increased (P < 0.0001). SBP was not significantly different between the CTEV and LOPE groups (P > 0.05). Terminal wire myography revealed that vessels from the NT group were more vasodilatory in response to acetylcholine (P = 0.0103) and less contractile in response to phenylephrine (P = 0.0435) and endothelin-1 (P < 0.0001). Vascular structure, cardiac function, and cardiac morphology were not different between all four T-EV groups. Exposure to T-EVs during pregnancy continued to influence maternal vascular function long after their administration. These findings confirm the role of T-EVs in regulating maternal vasculature long after the removal of the placenta at birth.NEW & NOTEWORTHY We have shown that normotensive T-EVs reduce blood pressure and promote a provasodilatory vascular phenotype for at least 12 mo after administration during pregnancy in a rat model. Administration of EOPE preeclamptic T-EVs prevented the natural decrease in blood pressure during pregnancy and increased blood pressure long-term. Together, these results suggest T-EVs play a key role in modulating maternal vascular function not only in pregnancy but also in determining future cardiovascular risk.
    Keywords:  extracellular vesicles; hypertension; placenta; preeclampsia; vascular dysfunction
    DOI:  https://doi.org/10.1152/ajpheart.00508.2026
  8. Hypertens Pregnancy. 2026 Dec 31. 45(1): 2734436
    Placental mitochondrial impairment in preeclampsia patients.
    Ramana Vaka, Elizabeth Hinton, Kristin Edwards, Babbette LaMarca.
      Preeclampsia is a pregnancy-specific hypertensive disorder characterized by new-onset hypertension after 20 weeks of gestation, accompanied by end-organ dysfunction with or without proteinuria. Affecting approximately 5-7% of pregnancies worldwide, it remains a leading cause of maternal and fetal morbidity and mortality. Despite decades of research, the underlying pathophysiology of preeclampsia remains incompletely understood. However, increasing evidence implicates placental mitochondrial oxidative stress in its pathogenesis. In this review, we summarize the current literature pertaining to ultrastructural evidence of mitochondrial damage, defects in oxidative phosphorylation and electron transport chain activity, and alterations in reactive oxygen species production, antioxidant defense, and mitochondrial biogenesis. Finally, we discuss translational considerations and highlight how therapeutic strategies targeted at restoring mitochondrial function may represent a promising approach for managing preeclampsia.
    Keywords:  Bioenergetics; mitochondria; placenta; preeclampsia; reactive oxygen species
    DOI:  https://doi.org/10.1080/10641955.2026.2734436
  9. Biol Bull. 2025 Oct;249(2-3): 92-111
    First Transcriptomic Insights into the Invertebrate Placental Analogue: Differential Gene Expression in Gonozooids of Crisiella producta (Bryozoa, Cyclostomatida).
    A Yu Kvach, V A Kutyumov, O N Kotenko, V V Starunov, A N Ostrovsky.
      AbstractPlacentotrophy, the most complex mode of nutrient transfer from a parental organism to developing embryos, has evolved multiple times among Metazoa, being a well-known example of convergent evolution. However, the molecular mechanisms underlying the development and physiology of placenta-like systems in invertebrates remain unknown. Phylum Bryozoa is an excellent model for studying the evolution of placentotrophy, since this reproductive strategy evolved repeatedly within this group. Cyclostome bryozoans are characterized by a unique syncytial/coenocytic placental analogue that nourishes polyembryonic progeny inside polymorphic zooids (gonozooids). Here, we provide transcriptomic analysis of the gonozooids in the cyclostome Crisiella producta. We generated a high-quality transcriptome assembly from reproducing colonies of C. producta and compared gene expression between feeding zooids and gonozooid developmental stages. Our analyses identified a core set of candidate transport proteins likely involved in nutrient delivery to progeny, as well as pronounced activation of extracellular matrix development and remodeling, consistent with ultrastructural data. Additionally, we tested the hypothesis of endocrine regulation in gonozooid development and revealed differential expression of insulin-like neuropeptides and the conserved nuclear receptor FTZ-F1. Together, these findings support the hypothesis that bryozoan placentotrophy is regulated by endocrine signaling, provide evidence for the transport function of the cyclostome placental analogue, and highlight the importance of the extracellular matrix in these processes.
    DOI:  https://doi.org/10.1086/743184
  10. Reprod Toxicol. 2026 Oct 21. pii: S0890-6238(26)00232-7. [Epub ahead of print] 109389
    Ellagic acid alleviates nicotine-induced placental injury in pregnant rats: Histomorphometric and molecular evidence.
    Zahra Gholamhoseinian, Kaveh Khazaeel, Jamal Nourinezhad, Javad Jamshidian.
      Maternal nicotine exposure during pregnancy is associated with placental dysfunction, oxidative stress, and impaired fetal development. Ellagic acid (EA), a naturally occurring polyphenolic compound with potent antioxidant properties, may protect placental tissues against nicotine-induced damage. This study investigated the protective effects of EA on placental histomorphometric alterations, oxidative stress, and apoptosis-related gene expression in nicotine-exposed pregnant rats. Twenty-four pregnant Wistar rats were randomly assigned to four groups (n = 6): control, EA (60mg/kg), nicotine (1mg/kg), and nicotine + EA. Treatments were administered orally from gestation day (GD) 0 to GD20. The H&E and PAS staining were used to evaluate placental architecture, trophoblast giant cells, and glycogen cell distribution. Oxidative stress biomarkers including MDA, CAT, TAC, SOD, and GPx were assessed. Expression levels of caspase-3, Bax, Bcl-2, and p53 genes were quantified using real-time PCR. Nicotine exposure significantly decreased the placental weight, diameter, and thickness characterized by disrupted placental architecture, changes in the thickness of placental layers, and the number of trophoblast giant cells (P<0.05). These changes were accompanied by increased lipid peroxidation, reduced antioxidant defense capacity, and dysregulation of apoptosis-related genes, including upregulation of caspase-3, Bax, and p53 and downregulation of Bcl-2. Co-administration of EA significantly attenuated these adverse effects by improving placental structural integrity, oxidative stress, and apoptosis-related genes expression (P<0.05). EA exerts significant protective effects against nicotine-induced placental injury, likely through its antioxidant and anti-apoptotic activities. These findings suggest that EA may represent a promising therapeutic strategy for mitigating placental toxicity associated with maternal nicotine exposure.
    Keywords:  Ellagic acid; Nicotine; Oxidative stress; Placenta; Pregnancy
    DOI:  https://doi.org/10.1016/j.reprotox.2026.109389
  11. Trends Endocrinol Metab. 2026 Oct 23. pii: S1043-2760(26)00276-6. [Epub ahead of print]
    Placental adaptation to maternal overnutrition as an evolutionary trade-off.
    Gernot Desoye, Jonathan C K Wells.
      The mammalian placenta is genetically identical to the fetus, exposing it to unique selective pressures. In humans, placental evolution has been explored through the lens of nutritional scarcity, with selective pressures assumed to diminish as resources increase. Here, we challenge this assumption, arguing that maternal overnutrition constitutes a distinct and underappreciated selective pressure. Maternal inability to maintain fuel homeostasis exposes the fetus to nutrient overload, elevating fetal insulin and oxygen demand. Selection has favored placental adaptive responses to the resulting oxygen deficit, with insulin as the mechanistic core. However, the role of fetal hyperinsulinemia in protecting brain oxygen supply comes at the cost of excess fetal adiposity. This trade-off carries downstream health risks, including obstetric risks, preterm birth, and intergenerational metabolic disease.
    Keywords:  diabetes; evolution; insulin-adaptive responses; obesity; oxygen; placenta
    DOI:  https://doi.org/10.1016/j.tem.2026.10.004
  12. Placenta. 2026 Oct 20. pii: S0143-4004(26)00723-X. [Epub ahead of print]186 189-198
    Maternal diet and placental outcomes: Evidence of sexual dimorphism among mothers with overweight and obesity.
    Shevaun M Teo, Alexander Douglass, James R Hébert, Celine M Murrin, Ricardo Segurado, Eileen O'Brien, Fionnuala M McAuliffe, Cecily C Kelleher, Catherine M Phillips.
       INTRODUCTION: Maternal diet may influence placental development and efficiency, reflected by placental weight (PW) and the birthweight-to-placental weight ratio (BW:PW). Mothers with overweight or obesity (OWOB) are at increased risk of adverse placental outcomes, yet evidence on maternal dietary influences on placental outcomes in OWOB remains limited.
    METHODS: We conducted secondary analysis of data on 423 mother-child pairs with maternal BMI ≥25 kg/m2 from two Irish cohorts (Lifeways Cross-Generation Cohort (n = 66) and the Pregnancy Exercise and Nutrition Research Study (PEARS) randomized controlled trial (n = 357)). Maternal diet in early pregnancy was assessed using food frequency questionnaires (Lifeways) and 3-day food diaries (PEARS). Dietary scores representing diet quality (HEI-2015, DASH, AHEI-P), inflammatory and antioxidant potential (E-DII, DII, DAQ), and glycemic and insulinemic characteristics (GI, GL, II, IL) were calculated. PW and birthweight were obtained from hospital records and BW:PW ratios were derived. Cohort-specific linear regression assessed dietary score associations with placental outcomes, including sex-stratified analyses.
    RESULTS: In Lifeways, higher general and pregnancy-specific DAQ scores were inversely associated with PW in fully adjusted models overall (B = -32.06 g and -29.73 g; p = 0.01) and among male (B = -39.77 g, p = 0.04 (DAQ)), but not female placentas. In sensitivity analyses of uncomplicated pregnancies in PEARS, II was positively associated with BW:PW ratio in females (B = 0.04, p = 0.04), while the DII was positively associated with male PW (B = 29.75 g, p = 0.02).
    CONCLUSIONS: Results suggest that maternal dietary patterns may be associated with placental growth in OWOB pregnancies, with potential sex-specific effects.
    Keywords:  Maternal dietary scores; Obesity; Overweight; Placental efficiency; Placental weight; Pregnancy; Sexual dimorphism
    DOI:  https://doi.org/10.1016/j.placenta.2026.10.006
  13. Nat Commun. 2026 09 17. pii: 10929. [Epub ahead of print]17(1):
    Multiplexed embryo profiling links cellular state to zygotic genome activation in single cells.
    Max Hess, Marvin F Wyss, Edlyn Wu, Gian-Marco Schaniel, Joel Lüthi, Chiara Rebagliati, Daniel Hannuschke, Nadine L Vastenhouw, Darren Gilmour, Shayan Shamipour, Lucas Pelkmans.
      Multicellular self-organization depends on interactions across multiple length scales, yet mapping protein states at high spatial resolution in whole-mount embryos remains challenging. Here, we introduce high-throughput 3D in toto iterative immunofluorescence imaging (3D-4i) and a dedicated computer vision pipeline to quantify morphological and molecular features from subcellular to whole-embryo scales across hundreds of samples. Applying this pipeline to early zebrafish embryos undergoing mid-blastula transition, we determine the cell cycle phase for each cell across the embryo, and uncover the spatiotemporal dynamics by which global meta-synchronous mitotic waves transition to cell cycle desynchronization. Using statistical analysis, we find that the cell cycle phase is the major source of variability in transcription within a division cycle, and combining this with the analysis of key transcription factors and chromatin modifier state, included in our multiplexed dataset, enables accurate prediction of transcriptional output during zygotic genome activation in individual cells. Together, these findings establish 3D-4i as a powerful approach for quantifying multimodal, multiscale biological processes underlying multicellular self-organization.
    DOI:  https://doi.org/10.1038/s41467-026-77784-7
  14. Physiol Rep. 2026 Oct;14(20): e71148
    Exercise in pregnant elite athletes: Physiological considerations, risks, and benefits.
    Ibelle Madera, Vedanti Bhargava, Jhillika Patel, Kritika Singh, Opal Jawale, Gloria Bachmann.
      The American College of Obstetricians and Gynecologists (ACOG) recommends engagement in moderate exercise throughout pregnancy, including aerobic and strengthening activities, which has been shown to offer numerous benefits during pregnancy. However, the intersection of pregnancy and athletics presents a unique set of challenges. ACOG guidelines on exercise during pregnancy primarily target recreational exercisers. Tailored recommendations are needed for pregnant elite athletes. This study examines both how pregnancy affects physiology and the risks/benefits of high-intensity exercise. Two independent reviews were conducted, using MESH search terms including "pregnant athletes," "female elite athlete," "maternal health," "exercise pregnancy." From 56 total studies, 40 studies with clinical data on over 4163 women, including elite athletes, were included in the review. Regular exercise during pregnancy can improve cardiovascular fitness and fetal vascular function while reducing risks of gestational diabetes, hypertensive disorders, delivering a large-for-gestational-age infant, and excessive weight gain. High-intensity activities can compromise fetal blood flow. Endurance athletes may safely maintain their training regimens during pregnancy, whereas those in high-altitude or contact sports require adjustments. Routine, non-intense exercise during pregnancy offers significant maternal and fetal health benefits. Future work should establish individualized recommendations supporting pregnant elite athlete health.
    Keywords:  fetal health; maternal health; physical exercise; pregnancy; sports
    DOI:  https://doi.org/10.14814/phy2.71148
This page is being maintained by Thomas Krichel. It was last updated on 2026‒10‒27 at 14:40.