Journal of Developmental Biology最新文献

{"title":"Evolutionary Analysis of Vertebrate KCNH Voltage-Gated Potassium Channels and Spatial Expression of <i>kcnh</i> Genes in Zebrafish Embryos.","authors":"Kuangyi Wu, Dingxun Wang, Ziyu Dong, Alice Yahui Zhou, GuangJun Zhang","doi":"10.3390/jdb14030032","DOIUrl":"10.3390/jdb14030032","url":null,"abstract":"<p><p>Voltage-gated potassium channels (Kv) are a large family of potassium channels composed of 40 members across 12 subtypes. The <i>KCNH</i> genes encode three subfamilies of voltage-gated potassium channels: Kv10 (EAG, <i>ether à go go</i>), Kv11 (ERG, EAG-related gene), and Kv12 (ELK, EAG-like K). Kv channels play prominent roles in neuronal and cardiovascular systems. Mutations in Kv channels have been linked to many human diseases, such as epilepsy, heart arrhythmias, and cancers. Significant progress has been made in understanding protein structures, physiological functions, and pharmacological modifiers. However, the evolutionary history and gene expression of vertebrate <i>KCNH</i> genes during embryonic development remain largely unknown. We systematically identified and cloned 14 <i>kcnh</i> genes in zebrafish. Then, we examined the vertebrate KCNH channel evolution by phylogenetic and syntenic analyses. Our data reveal that the three subtypes of the <i>KCNH</i> gene family had already evolved in invertebrates, long before the emergence of vertebrates. The number of vertebrate <i>KCNH</i> genes increased, most likely due to whole-genome duplications (WGDs). In addition, we examined zebrafish <i>kcnh</i> gene expression during early embryogenesis by in situ hybridization. Each subgroup's genes showed similar but distinct gene expression domains with some exceptions. Most of them were expressed in neural tissues. Notably, <i>kcnh6a</i> showed robust expression in the developing heart, consistent with its conserved role in cardiac repolarization. Additionally, a few <i>kcnh</i> genes were transiently expressed in non-neural tissues, such as somites and the notochord, suggesting they may have a unique role in embryonic development. Our phylogenetic and developmental analyses of KCNH channels shed light on their evolutionary history and potential roles during embryogenesis, in line with their physiological functions and human channelopathies.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398235/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148578738","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":"CSF1R+ Macrophages and Osteoclasts Are Essential for Limb Bone Development During Embryogenesis.","authors":"Felix Ma, Rose Ru Jing Zhou, Matthew Rosin, Jessica M Rosin","doi":"10.3390/jdb14030031","DOIUrl":"10.3390/jdb14030031","url":null,"abstract":"<p><p>Colony-stimulating factor-1 receptor (CSF1R) provides essential signals for macrophage and osteoclast proliferation, differentiation, and survival, but the roles of CSF1R+ macrophages and osteoclasts during limb morphogenesis are understudied. Here, we utilized a pharmacological model by feeding the CSF1R inhibitor PLX5622 to pregnant mice across gestation to examine how CSF1R disruption impacts embryonic limb development. CSF1R-expressing cells were significantly depleted in response to PLX5622 exposure, including a complete loss of embryonic osteoclasts and osteoclastic activity in the developing limb bones. Although the gross morphology of limb nerves, muscles, cartilage, and bone appeared intact between embryonic day 11.5 (E11.5) and E15.5, prenatal PLX5622 exposure resulted in a completely penetrant truncated phenotype for all postnatal day 1 (P1) limb bones analyzed, suggesting that CSF1R+ cells play important roles in mediating limb bone formation during late embryogenesis. Interestingly, strain-specific defects were observed in the heel, where most of the CD1 mice presented with absent talus and underdeveloped calcaneus bones, while the C57BL/6 mice presented with milder developmental disruptions in both bones. Taken together, our data demonstrate that PLX5622 effectively depletes CSF1R-expressing macrophages and osteoclasts in embryonic limbs and suggest an essential role for embryonic CSF1R+ cells in driving limb bone morphogenesis.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13397857/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148578686","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":"Valproic Acid Induces Post-Translational Redox Modifications in Mouse Embryos That Are Prevented via Prior Nrf2 Activation.","authors":"Aubrey Johansen, Kendall Dunford, Garrett Hasegawa, Jason M Hansen","doi":"10.3390/jdb14030030","DOIUrl":"10.3390/jdb14030030","url":null,"abstract":"<p><p>Valproic acid (VPA) is a human developmental toxicant that causes neural tube defects and neurobehavioral deficits. Recent work has implicated VPA-induced oxidative stress in cell models of neurodifferentiation, where oxidative post-translational modifications (PTMs) in undifferentiated cells, primarily protein sulfenylation (Pr-SOH), were unique compared to differentiated neurons, primarily protein S-glutathionylation (Pr-SSG). Many of these effects could be mitigated by pretreatments with an Nrf2 inducer. However, it is unclear how early-stage mouse embryos (gestational day 8.5) respond to VPA treatments. Using whole embryo culture, mouse embryos were treated with VPA. A time course assessment of glutathione/glutathione disulfide redox potentials was performed via HPLC throughout 24 h of culture. At 6 h of VPA treatment, embryos were collected for the assessment of protein redox states and specific protein PTMs via various blotting techniques. Also, at 6 h of treatment, the localization of specific PTMs was determined via whole mount staining. Some embryos were pretreated with an Nrf2 inducer. Our data demonstrated that VPA caused a sharp oxidation of redox potentials, which were the greatest between 2 and 6 h, but reverted to control levels by 24 h. Preemptive Nrf2 activation prevented VPA-induced oxidation. Redox blotting showed that VPA caused oxidation of the proteome but this could be reversed by D3T pretreatment. More specifically, Pr-SOH levels increased but Pr-SSG levels were unchanged. Increased Pr-SOH could also be reversed with prior Nrf2 activation. We conclude that embryos at these early stages of development are highly sensitive to VPA and respond more like undifferentiated cells, promoting a more pro-oxidizing outcome for proteins, increasing Pr-SOH formation vs. Pr-SSG. These findings may support specific windows of development where embryos are more susceptible to VPA-induced oxidative injury. Further understanding of redox control and regulation at these susceptible states may serve to develop preventative strategies to reduce poor developmental outcomes after exposures.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398012/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148578735","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":"Wee Kinases, Big Impact: Wee and Myt Kinases as Critical Regulators of Meiotic Progression.","authors":"Shannon Pfeiffer, Lourds M Fernando, Anna K Allen, Aimee Jaramillo-Lambert","doi":"10.3390/jdb14030029","DOIUrl":"10.3390/jdb14030029","url":null,"abstract":"<p><p>Regulation of the cell cycle is critical for maintaining genomic integrity. Therefore, cells have adapted several mechanisms to ensure that cell cycle events occur in a precise order. Some mechanisms regulate cell cycle progression by inhibiting cell cycle drivers, cyclin-dependent kinases (CDKs). The Wee1/Myt1 family of kinases regulate the G2-to-M phase transition by phosphorylating and inactivating Cdk1. Investigations of Wee1/Myt1 have mainly focused on its regulation of mitosis; the role of Wee1/Myt1 kinases in the meiotic cell cycle is less well understood. However, misregulation of Wee1/Myt1 during meiosis can have a range of fertility consequences from mild to severe, including human fertilization failure and infertility. Studies from several organisms reveal that the meiotic functions of Wee1/Myt1 kinases differ from mitosis depending on the species and sex. Here, we review how Wee1/Myt1 kinases regulate cell cycle progression in meiosis across species. We highlight current knowledge of Wee1/Myt1 in meiosis and discuss unanswered questions and new directions to advance the field of meiosis and reproduction. Understanding the molecular and cellular functions of Wee1/Myt1 homologs in these various systems may contribute to the discovery of the mechanisms underlying human infertility cases, better diagnoses, and clinical treatments.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 3","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398180/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148578732","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":"An Overview of How Epigenetics, MicroRNA-21, and Endocrine Disrupting Compounds Affect Oocyte Maturation and Pre-Implantation Embryo Development.","authors":"Monique Nasser, Reem Sabry, Laura A Favetta","doi":"10.3390/jdb14020028","DOIUrl":"10.3390/jdb14020028","url":null,"abstract":"<p><p>Epigenetic regulation is pivotal in reproductive processes, such as oocyte maturation and pre-implantation embryonic development, and it impacts gene expression without altering DNA sequence through mechanisms including DNA methylation, histone modifications, and non-coding RNAs. Primarily, microRNA-21 is involved in meiotic progression, apoptosis, and cumulus cell function, which are necessary for oocyte competency. miR-21 dysregulation can lead to improper oocyte maturation and poor embryonic development, ultimately causing developmental defects. During pre-implantation embryonic development, DNA methylation and histone modifications contribute to cellular reprogramming, ensuring proper gene activation and repression. Environmentally, endocrine disruptors affect miR-21 expression, potentially disrupting pathways involved in reproductive health and developmental programming. Overall, this review explores the correlation between epigenetics, miRNA regulation, and environmental factors, emphasizing the intricacies of oocyte maturation and pre-implantation embryonic development. This highlights the need for additional mechanistic and translational research in reproductive epigenetics.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 2","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13301040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148317322","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":"The Gut Microbiome in Early Ontogeny: Implications for Brain and Immune System Development.","authors":"Alejandro Borrego-Ruiz, Juan J Borrego","doi":"10.3390/jdb14020027","DOIUrl":"10.3390/jdb14020027","url":null,"abstract":"<p><p>The gut microbiome plays a pivotal role in modulating multiple physiological processes from the earliest stages of life. However, the complete scope of its effects during childhood is yet to be fully elucidated, which underscores the importance of enhancing the understanding of this emerging area of research. This narrative review provides an overview of the influence of the gut microbiome in early human ontogeny by examining its role in brain and immune development, as well as its involvement in neurodevelopmental disorders and early-life mental health. The gut microbiome contributes to shaping the development and function of both the brain and the immune system. Its influence appears to be primarily mediated through the synthesis of neurotransmitters and microbial metabolites, as well as through the activation of specific pathways within the hypothalamic-pituitary-adrenal axis. Nevertheless, the exact mechanisms through which the gut microbiome exerts these effects, and the full extent of its impact on neurodevelopmental and immune health, remain incompletely understood and continue to be active areas of research and scientific debate. Ultimately, advances revealing how the gut microbiome shapes early brain and immune system development will create new opportunities for innovative interventions and predictive strategies aimed at transforming pediatric health outcomes.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 2","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13301301/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148317335","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":"Gestational Dynamics of Hofbauer Cells in the Human Placenta: Distribution, Morphology, and Immunophenotype.","authors":"Sanja Jovičić, Ivan R Nikolić, Ljiljana Božić, Marko Jović, Dina Kapić, Ranko Škrbić","doi":"10.3390/jdb14020026","DOIUrl":"10.3390/jdb14020026","url":null,"abstract":"<p><strong>Background: </strong>Hofbauer cells (HBCs) are the only immunocompetent cells within the stroma of chorionic villi and play a key role in immune regulation and placental development throughout gestation. Their phenotype, abundance, and proliferative activity change in accordance with the needs of the fetoplacental unit.</p><p><strong>Methods: </strong>Thirty healthy human placentas across all three trimesters were analyzed. Samples were processed using standard histological protocols and immunohistochemically stained with CD45, CD68, CD86, and Ki-67 markers. Morphometric analysis was performed to determine the following parameters: percentage of HBCs, numerical areal density, and proliferative index.</p><p><strong>Results: </strong>HBCs were immunoreactive for CD45 and CD68, while CD86 immunoreactivity was not observed in any trimester. The proportion of HBCs was highest in the second trimester and lowest in the third. Numerical areal density was highest in the second trimester (22.21 ± 3.86) and lowest in the first (8.27 ± 4.18). The proliferative index was highest in the first trimester (82.45 ± 10.19%), decreased significantly in the second, and was completely absent in the third trimester.</p><p><strong>Conclusions: </strong>During physiological placental development, Hofbauer cells maintain a predominantly non-M1 macrophage phenotype, accompanied by a gradual reduction in proliferative activity.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 2","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13301675/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148317343","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":"Spatiotemporal Profiling Defines the Epithelial and Mesenchymal Transition Window in Embryonic Lung Morphogenesis.","authors":"Huiwen Zheng, Jinpei Lin, Hanyi Li, Shijie Hao, Mengnan Cheng","doi":"10.3390/jdb14020025","DOIUrl":"10.3390/jdb14020025","url":null,"abstract":"<p><p>Lung organogenesis is orchestrated by dynamic epithelial-mesenchymal interactions during embryogenesis, yet the gene regulatory programs and signaling dynamics governing these processes in the pseudoglandular stage remain incompletely understood. In this study, we integrated spatial and single-cell transcriptomic data across embryonic developmental stages to systematically characterize epithelial and mesenchymal dynamics during lung development. To achieve more refined cell types at single-cell resolution in spatial transcriptomic data, we developed a bin-based deconvolution strategy that enabled high-precision cell-type assignment. We subsequently constructed a 3D spatiotemporal landscape of lung development and elucidated the molecular regulatory mechanisms underlying epithelial-mesenchymal maturation during lung morphogenesis. In addition, we analyzed transcription factor module activity, intercellular communication signaling, and predicted downstream target genes, while integrating public GWAS metadata to link developmental programs with lung cancer-related features. We observed pronounced stage-specific functional heterogeneity between the pseudoglandular and late embryonic stages. Notably, E13.5 emerged as a critical transition window, during which progenitor states shifted toward more mature cellular phenotypes. We reconstructed epithelial-mesenchymal interactions and uncovered coordinated rewiring of ligand-receptor signaling and transcriptional networks across developmental stages. Regulatory network analysis further identified temporally coordinated transcription factor modules centered on <i>Tbx3</i>, <i>Tbx5</i>, <i>Gli1</i>, <i>Gata4/5</i>, <i>Foxa1/2</i>, and <i>Cebpa</i>, which collectively orchestrated branching morphogenesis, epithelial patterning, and tissue stabilization. Integration with lung cancer genome-wide association data demonstrated that embryonic lung progenitor states exhibit strong associations with lung cancer-related transcriptional programs, particularly involving epithelial-mesenchymal plasticity and RNA-splicing pathways. Furthermore, TP53/HNRNP-mutant lung adenocarcinomas displayed embryonic-like molecular features associated with cytoskeletal remodeling and progenitor-state reactivation. Together, our study provided a spatiotemporally resolved framework of embryonic lung development and identifies a critical transition window linking lung morphogenesis, regulatory network remodeling, and cancer-associated epithelial plasticity.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 2","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13300856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148317299","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":"The Association Between the Progressive Motility of Bovine Spermatozoa and the Developmental Morphokinetics of In Vitro-Derived Embryos.","authors":"Shir Maizus, Dorit Kalo, Tanya Kogan, Ariel Michaelov, Zvi Roth","doi":"10.3390/jdb14020024","DOIUrl":"10.3390/jdb14020024","url":null,"abstract":"<p><p>The proportion of spermatozoa with progressive motility is widely used to evaluate the quality of a single ejaculate. However, the cellular and physiological mechanisms underlying this trait remain unclear. The present study examined the association between the progressive motility of bovine spermatozoa, their quality and their fertilization competence in vitro, and subsequently the association with the developmental morphokinetics of the formed embryos. Fresh ejaculates were classified and divided into groups with high (HPM), medium (MPM), or low (LPM) progressive motility. Then, spermatozoa were evaluated for their morphology, plasma membrane integrity, mitochondrial membrane potential, oxidative status, and acrosome integrity. The findings revealed that spermatozoa from HPM ejaculates enhanced motility in association with higher mitochondrial membrane potential relative to the LPM group, suggesting higher metabolic potential. No differences were recorded in fertilization competence among groups; however, the developmental kinetics of the formed embryos, determined by a time-lapse system, differed; embryos derived from HPM spermatozoa cleaved earlier to the two-, three-, and four-cell stages than embryos derived from MPM spermatozoa, suggesting that HPM-derived embryos are of good quality. Our findings suggest that progressive motility is not only a motility characteristic; it also reflects cellular quality of spermatozoa and the formed embryo.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 2","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13214785/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148031315","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":"Expression and Role of Colony Stimulating Factor 1 Receptor During Odontogenesis.","authors":"Ashina Nagra, Ling-Yi Chen, Soheil Saeidiborojeni, Jessica M Rosin, Siddharth R Vora","doi":"10.3390/jdb14020023","DOIUrl":"10.3390/jdb14020023","url":null,"abstract":"<p><p>In osteopetrotic mice with homozygous inactivating mutations in the colony stimulating factor 1 (<i>Csf1^op/op</i>) or its receptor (<i>Csf1r^-/-</i>) gene, teeth fail to erupt due to severe reduction in osteoclastogenesis. Dental abnormalities have been described in the unerupted teeth of these models, but it remains unclear whether these defects arise from direct roles of CSF1R in odontogenesis or indirectly from impaired bone remodeling associated with failed eruption. Here, we examined the spatiotemporal expression of CSF1R during tooth development and inhibited CSF1R pharmacologically in utero using PLX5622 during early stages of tooth morphogenesis. Teeth and surrounding bone were analyzed at embryonic and postnatal stages using histology and high-resolution micro-computed tomography. Embryonic CSF1R inhibition resulted in reproducible abnormalities in incisor and molar morphology that were evident before and after birth and were associated with loss of normal bone remodeling at the tooth-bone interface. In contrast, postnatal CSF1R inhibition did not affect the structure or continuous growth of adult incisors. Together, these findings demonstrate a temporally restricted, indirect role for CSF1R in odontogenesis that is independent of tooth eruption and associated with remodeling of the bony crypts surrounding developing teeth by CSF1R-dependent cells.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 2","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13214697/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148031287","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}