Journal of Developmental Biology最新文献

{"title":"PBX3 Promotes Oligodendrocyte Progenitor Cell Proliferation and Differentiation During Early Postnatal Development.","authors":"Yanling Yang, Jing Ling, Zhongzhe Zhang, Jie Yuan, Kaixiang Zhang, Xiang Xiao, Hui Guo, Ming Zhang, Xianghui Zhao","doi":"10.3390/jdb14030042","DOIUrl":"10.3390/jdb14030042","url":null,"abstract":"<p><p>Pre-B-cell leukemia transcription factor 3 (PBX3) is a TALE homeodomain protein involved in neural development, but its function in oligodendrocyte (OL) differentiation has remained unexplored. Here, we show that PBX3 expression is dynamically regulated during OL lineage progression, with peak expression in the corpus callosum at P14, corresponding to the onset of active myelination. In cultured primary oligodendrocyte precursor cells (OPCs), PBX3 expression peaked at OL-1DIV, an early stage of in vitro differentiation. Using OL lineage-specific <i>Pbx3</i> conditional knockout mice, we found that <i>Pbx3</i> deletion reduced the density of SOX10⁺ OL lineage cells and CC1⁺ mature OLs in the corpus callosum at P14 and P27, accompanied by decreased MBP expression. Notably, these deficits were largely resolved by P50, indicating an age-dependent rather than absolute requirement for PBX3. EdU labeling revealed reduced OPC proliferation in <i>Pbx3</i> cKO mice, though the <i>Olig1-Cre</i> driver used for conditional deletion is active in early neural progenitors, and thus contributions from reduced OPC specification or generation cannot be excluded. Consistently, siRNA-mediated <i>Pbx3</i> knockdown in primary OPCs impaired differentiation and reduced MBP expression in vitro. Collectively, our findings identify PBX3 as a positive regulator of OL differentiation during early postnatal development, with a temporally restricted requirement, and provide insights into the transcriptional control of CNS myelination.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13608693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Akhirin Preserves Hemostatic Wound Repair Through Non-Hematopoietic Regulation of the Vascular Injury Microenvironment.","authors":"Mohammad Badrul Anam, Mikiko Kudo, Terumasa Umemoto, Keisuke Yamashita, Rie Kawano, Kunimasa Ohta","doi":"10.3390/jdb14030041","DOIUrl":"10.3390/jdb14030041","url":null,"abstract":"<p><p>Hemostasis and wound healing are highly coordinated processes that involve rapid clot formation followed by controlled remodeling of the injured tissue microenvironment. Prior work on Akhirin (AKH), a secreted extracellular matrix protein containing two von Willebrand factor A domains and an LCCL domain, has established it as a regulator of the neural stem niche in the developing brain and spinal cord injury microenvironment. However, its role as a non-hematopoietic molecule in the vascular injury response remains unknown. Here, we present evidence that AKH contributes to hemostasis and wound repair outside the neural niche. Our immunohistochemical and biochemical analyses demonstrated AKH around arterial tissues, suggesting a potential role at the blood-vessel interface. AKH-deficient mice exhibited a striking phenotype characterized by prolonged tail bleeding and delayed wound closure, indicating impaired vascular injury repair in vivo. Furthermore, bone marrow transplantation failed to rescue the prolonged bleeding phenotype, supporting a predominant non-hematopoietic contribution. Intriguingly, analysis of classical coagulation revealed an apparent paradox: activated partial thromboplastin time was shortened, whereas prothrombin time was not significantly altered. In contrast, increased expression of tissue plasminogen activator, urokinase-type plasminogen activator, and urokinase-type plasminogen activator receptor in AKH-deficient samples suggested dysregulated local fibrinolytic remodeling. Together, these findings identify AKH as a previously unrecognized extracellular regulator of hemostatic wound repair. Rather than indicating a defect in classical coagulation cascade activation, the findings associate AKH deficiency with impaired hemostatic control and altered expression of plasminogen activator system components, suggesting a role for AKH in the local vascular injury response.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13608595/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diaphragmatic Mitochondrial Myopathy in a Patient-Derived Mouse Model of Barth Syndrome.","authors":"Kristen Tentler, Paige L Snider, Catalina Matias, Jeffrey J Brault, Simon J Conway","doi":"10.3390/jdb14030040","DOIUrl":"10.3390/jdb14030040","url":null,"abstract":"<p><p>Barth syndrome (BTHS) is a rare, X-linked genetic disorder caused by mutations in the enzyme TAFAZZIN (TAZ), resulting in insufficient cardiolipin (CL) remodeling and mitochondrial dysfunction. While BTHS respiratory distress and breathing difficulties are commonly reported, the precise role of intrinsic respiratory tissue vulnerabilities has only recently begun to be appreciated. Historically, BTHS respiratory distress is frequently attributed to secondary consequences like cardiomyopathy or generalized skeletal myopathy, leaving the intrinsic vulnerability of vital respiratory muscles poorly understood. Using a patient-tailored point mutant knock-in mouse model (<i>Taz^PM</i>) harboring a stable but enzymatically deficient Taz^D75H protein, we investigated the autonomous physiological and metabolic responses in the diaphragm and lungs. Contrary to the paradigm that respiratory muscles are unaffected, <i>Taz^PM</i> diaphragms exhibit structurally abnormal mitochondria and undergo a survival-critical, bifurcated compensatory remodeling response to prevent fatal respiratory failure under severe bioenergetic stress. The <i>Taz^PM</i> adaptive mechanism is orchestrated by chronic activation of the mitochondrial Integrated Stress Response (ISR) via the Gcn2/eIF2α signaling pathway. This stress pathway halts global translation to conserve cellular ATP at the expense of reduced NAD+ levels, while selectively upregulating defensive mitokines and metabolic sirtuins and structural muscle remodeling. Furthermore, the <i>Taz^PM</i> diaphragm transitions into a highly specialized, slow-twitch motor system that is expected to reduce the energy cost per contraction. Concurrently, despite <i>Taz^PM</i> lungs exhibiting structurally abnormal mitochondria, they resist generalized mitochondrial collapse despite ADP reduction, executing tissue-specific metabolic reprogramming and localized biochemical adaptations to sustain respiratory homeostasis.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13608765/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of a Novel Fluorescent Marker for Continuous Live Imaging of Preimplantation Embryos.","authors":"Debbie Montjean, Karine Audette, Simon Mathien, Marie-Hélène Godin-Pagé, Moncef Benkhalifa, Ibrahim Bilem, Pierre Miron","doi":"10.3390/jdb14030039","DOIUrl":"10.3390/jdb14030039","url":null,"abstract":"<p><p>This study evaluates ChromaLIVE^TM, a multichromatic, mix-and-read fluorescent marker developed for continuous live-cell imaging, in the context of embryology. The aim was to evaluate whether this marker is compatible with dynamic embryonic development up to the blastocyst stage, with minimal impact on embryo viability, integrity, or normal growth of mouse embryos at the 2-cell stage that were cultured to the blastocyst stage under time-lapse imaging conditions, either in the presence or absence of ChromaLIVE^TM. Results showed comparable blastocyst formation rates between ChromaLive^TM and the control group, as well as similar proportions of high-quality blastocysts. Although minor but statistically significant delays were noted in two kinetics events (t3 and tSB), other developmental timings remained unaffected. Time-lapse confocal fluorescence imaging demonstrated that ChromaLIVE^TM dye provided stable, bright, high-resolution 3D visualizations of cellular compartments including membranes, cytoplasm and embryonic structures such as trophectoderm, inner cell mass and blastocoel throughout development. Finally, transcriptomic analyses revealed a limited set of gene-expression differences between stained and unstained embryos; although these included developmental and metabolic pathways, embryos developed to the blastocyst stage comparably to controls.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13607945/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNAs as Regulators of Reproductive Function: From Gametogenesis to Pregnancy.","authors":"Sabrina Roy, Karina Gutierrez, Vilceu Bordignon, Werner Giehl Glanzner","doi":"10.3390/jdb14030038","DOIUrl":"10.3390/jdb14030038","url":null,"abstract":"<p><p>The regulation of transcriptional activity constitutes a primary layer of control over cellular function across diverse tissues and cell types. This regulatory transcriptional landscape is largely governed by epigenetic mechanisms, including DNA and histone modifications, the dynamic activity of epigenetic \"writers\" and \"erasers,\" and the influence of small regulatory molecules such as microRNAs (miRNAs). miRNAs are small non-coding RNA molecules that play critical roles in transcriptional and post-transcriptional gene regulation. By modulating the expression of transcription factors, kinases, and other regulatory proteins, miRNAs exert tight control over cellular processes and maintain homeostasis. Given the essential requirement for precise cellular coordination in reproductive biology, miRNAs have emerged as key regulators of reproductive function. They participate in multiple stages of reproductive processes, ranging from ovarian function to the establishment and maintenance of pregnancy, thereby influencing fertility outcomes across species. In this review, we summarize recent advances in understanding the roles of miRNAs in key reproductive events, including gametogenesis, oocyte maturation, embryonic genome activation, early embryonic development, implantation and pregnancy. We aim to highlight the principal miRNAs involved in the maintenance of reproductive function and fertility, and their molecular targets and the regulatory networks when known. Based on our review, we conclude that although their potential in clinical and/or agricultural applications still remains uncertain, their role in regulating fundamental aspects of cellular biology, particularly reproductive processes, is becoming increasingly clear.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13607707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regionally Distinct Modes of Intestinal-Systemic Vascular Connections in Developing Zebrafish.","authors":"Akihiro Urasaki, Koichi Kawakami, Osamu Nakagawa","doi":"10.3390/jdb14030037","DOIUrl":"10.3390/jdb14030037","url":null,"abstract":"<p><p>Connecting the intestinal vasculature with the pre-existing systemic circulatory system is vital for nutrient absorption and blood transport for detoxification in the liver. However, the cellular processes underlying this connection remain unclear. Using genetically modified zebrafish models and in vivo imaging, we visualized that the supra-intestinal artery (SIA) connected to the pre-existing dorsal aorta (DA) in two distinct regions, the anterior and posterior. We found that endothelial cells migrated out of the DA and formed the anterior SIA-DA junction, whereas endothelial cells sprouted from SIA and connected to the DA in the posterior region. Pharmacological and genetic analyses revealed that activin receptor-like kinase 1 (ALK1) signaling was required for the SIA-DA connections. The present study provides new insights into the cellular phenomena and regulatory mechanisms of intestinal vascular development.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13511000/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148829147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modeling Complex Developmental Disease: The Case of Polycystic Kidney Disease.","authors":"Jay DeLoriea, Cody Casey, Lexee Shearer, Victoria Chen, Angelica Bryant, Chiara Gamberi","doi":"10.3390/jdb14030036","DOIUrl":"10.3390/jdb14030036","url":null,"abstract":"<p><p>Both genetics and the environment affect the phenotypes of polycystic kidney diseases (PKD), such as autosomal dominant (AD) PKD, autosomal recessive (AR) PKD and nephronophthisis (NPH). Variable phenotypes, pleiotropy, divergent severity and progression, even in family members who inherited the same disease-causing mutation(s), signal the involvement of networked genes and modifiers. Several PKD-linked genes function in development and renal tubule morphogenesis. Cystic renal tissues feature metabolic remodeling, functional reprogramming and dysregulation of several shared factors and pathways. ADPKD, ARPKD and NPH partially phenocopy each other. Understanding the developmental arc of cystic kidney disease and its complex phenotypes would improve diagnostics and help develop effective personalized treatments. However, this is challenging to study in vertebrate systems due to genetic redundancy, functional overlap, and a dearth of genetic tools. Underused in this context, <i>Drosophila melanogaster</i> offers high genomic and pathway conservation, a wealth of genetic tools, and rapid generation times, making it a reliable and sustainable model for mechanistic, genome-wide, and precision medicine studies. Here, we surveyed ADPKD, ARPKD, and NPH, compared renal and extrarenal phenotypes, and examined the network of shared and unique contributors, their healthy and diseased functions and conservation from the perspective of mechanistic whole-animal modeling.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13510785/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148829125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Speculations on the Evolution of Tail Regeneration in Lizards: Lessons from an Outstanding Case of Organ Regeneration in Amniotes.","authors":"Lorenzo Alibardi","doi":"10.3390/jdb14030035","DOIUrl":"10.3390/jdb14030035","url":null,"abstract":"<p><p>Based on updated information on tail regeneration in lizards, a hypothesis is introduced to explain why these reptiles evolved their regenerative ability. The hypothesis, supported by paleontological evidence, considers tail regeneration associated with autotomy since the Paleozoic in amphibian anthracosaurs of the Carboniferous Period. It is submitted that these ancient amphibians developed tails containing stem cells localized in autotomous planes and/or inter-muscle connective tissues, from which they could regenerate their tails, as some extant salamanders do. The process of stem cell distribution during vertebrate development in salamanders and lizards, however, remains to be demonstrated. It is here suggested that autotomy and regeneration were inherited in the reptiliamorph basal amniotes of the Upper Carboniferous, then in captorhinids of the Permian, in eosuchians of the Triassic, and in the derived Mesozoic lizards, allowing survival and radiation into numerous families. Only in a few lizard families, perhaps under specific ecological adaptations, was autotomy lost, reducing or eliminating tail regeneration. Transcriptome analysis of developing versus regenerating tail indicates numerous differences, suggesting that regeneration utilizes alternative developmental gene pathways from those activated during development. Clarification of gene networks evolved for lizard tail regeneration may indicate the essential steps necessary to regenerate organs also in other amniotes.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13510543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148829095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Frameshift Mutations in Exon 1 of <i>Fgf10</i> Frequently Yield Morphologically Normal Embryos.","authors":"Khanui Lkhagvadorj, Eiichi Okamura, Toshifumi Morimura, Seiya Mizuno, Masatsugu Ema","doi":"10.3390/jdb14030033","DOIUrl":"10.3390/jdb14030033","url":null,"abstract":"<p><strong>Background/objectives: </strong>CRISPR/Cas9-mediated genome editing enables efficient generation of knockout mouse models; however, frameshift mutations do not always result in complete loss of function. The factors influencing functional inactivation following frameshift mutations remain incompletely understood. Here, we tested whether frameshift-dominant targeting of exon 1 is sufficient to generate a null allele of <i>Fgf10</i>, a gene essential for limb formation.</p><p><strong>Methods: </strong>Guide RNAs (gRNAs) were selected using a machine learning-based pipeline to favor microhomology-mediated end joining (MMEJ)-dominant repair. Editing efficiency and indel profiles were assessed via amplicon sequencing in mouse embryonic stem cells (mESCs) and preimplantation embryos. Edited embryos were transferred to surrogate females and analyzed at embryonic day 15.5 (E15.5).</p><p><strong>Results: </strong>Amplicon sequencing confirmed >97% editing efficiency and >80% frameshift alleles in both mESCs and preimplantation embryos, with a predominant 7 bp deletion. Despite highly efficient frameshift-dominant editing, most of the E15.5 embryos were morphologically normal, indicating that exon 1 targeting did not reliably produce null phenotypes. In silico analysis suggested the possible presence of alternative downstream translation initiation sites, and our secretion assay supported this possibility. Initiation from a downstream ATG in a +2 reading frame (e.g., 7 bp deletion) may restore the downstream coding sequence and partially preserve protein function.</p><p><strong>Conclusions: </strong>Frameshift mutations in exon 1 of <i>Fgf10</i> do not consistently result in functional knockout. The functional outcome depends on the specific reading frame and may be influenced by alternative translation initiation and protein domain architecture. These findings highlight important considerations for designing genome editing strategies to achieve complete gene inactivation.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13511607/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148829115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Warfarin-Induced Developmental Toxicity: Insights into Embryogenesis, Teratogenicity, and Molecular Pathways.","authors":"Evelyn Magee, Grace Kuhnel, Poongodi Geetha-Loganathan","doi":"10.3390/jdb14030034","DOIUrl":"10.3390/jdb14030034","url":null,"abstract":"<p><p>Warfarin is a coumarin-derived oral anticoagulant widely used for the prevention and treatment of thromboembolic disorders, particularly in patients with mechanical heart valves. The drug exerts its anticoagulant effect by inhibiting vitamin K epoxide reductase, thereby impairing γ-carboxylation of vitamin K-dependent coagulation factors. Despite its clinical efficacy, warfarin therapy is associated with a narrow therapeutic index, substantial interindividual variability in dose response, numerous drug interactions, and significant hemorrhagic risk. Maternal warfarin therapy during pregnancy is strongly associated with fetal warfarin syndrome (FWS), a characteristic pattern of embryopathy resulting from in utero exposure to the drug. This review summarizes current knowledge regarding the physicochemical properties, pharmacological mechanisms, dose variability, toxicity, and developmental effects associated with warfarin exposure. Evidence from human clinical studies and vertebrate animal models is discussed to elucidate conserved developmental and molecular mechanisms underlying warfarin teratogenicity. The review also examines the signaling pathways disrupted by warfarin exposure, highlighting that its teratogenic effects extend beyond anticoagulation to the disruption of vitamin K-dependent developmental signaling. Inhibition of γ-glutamyl carboxylation, together with alterations in Gas6/TAM, PXR, Ras, and Wnt/β-catenin signaling pathways, impairs skeletal, vascular, and neural development, contributing to the characteristic abnormalities of fetal warfarin syndrome. Collectively, this review integrates clinical, molecular, and experimental findings to provide a comprehensive understanding of warfarin-induced developmental toxicity. Current knowledge is insufficient to fully elucidate the complex mechanisms underlying warfarin-induced embryopathy and fetal toxicity. Further investigations are warranted to identify safer anticoagulant regimens during pregnancy and to inform the development of novel therapeutic strategies that minimize fetal risk while maintaining maternal anticoagulation.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13511227/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148829242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}