Molecular Neurobiology最新文献

{"title":"SnRNA-seq Interprets Mechanisms by which Three Glial Cell Types Influence Myelin Regeneration in Adult Drug-Resistant Epilepsy-Related Cognitive Impairment.","authors":"Lu Wang, Jia-Qi Ma, Yong-Qian Bian, Xiao-Peng Qu, Yue Zhang, Chao Wang, Guo-Dong Gao, Long-Long Zheng, Qi-Xing Fang, Li-Jia Song, Liang-Liang Shen, Bei Liu","doi":"10.1007/s12035-025-05206-8","DOIUrl":"10.1007/s12035-025-05206-8","url":null,"abstract":"<p><p>Myelin regeneration has been shown in previous studies to ameliorate varying degrees of cognitive impairment in patients with neurodegenerative disorders such as epilepsy. The problem of myelin regeneration in adults with drug-resistant status epilepticus is a major key to the difficulty of treating cognitive impairment in adults with drug-resistant epilepsy (DRE). The purpose of this study is to provide a molecular map of myelin-related molecules under the cognitive deficits seen in DRE. We used a lamotrigine-pentylenetetrazol-resistant epilepsy mouse model and verified the cognitive problems and myelin changes using a water maze and conventional molecular biology techniques. We then analyzed the OLs in the hippocampus of the mice and the effect on myelin using sn RNA-seq technology. We found that the problem of cognitive impairment in drug-resistant epileptic mice is due to altered myelin plasticity. OL maturation induces pathological myelin regeneration which ultimately leads to cognitive impairment. The three glial cell types are closely related to the occurrence of myelin regeneration and jointly promote pathological myelin regeneration. Our study revealed the presence of myelin regeneration in DRE. All of this evidence suggests that normal myelin regeneration contributes to cognitive impairment improvement, but pathological myelin regeneration impairs cognition.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14196-14220"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511217/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144659675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hippocampal Interneurons Shape Spatial Coding Alterations in Neurological Disorders.","authors":"Juliane Midori Ikebara, Renata Silva Jorge, Luciana Simões Rafagnin Marinho, Guilherme Shigueto Vilar Higa, Avishek Adhikari, Fernando M C V Reis, Fernando S Borges, Henning Ulrich, Silvia Honda Takada, Roberto De Pasquale, Alexandre Hiroaki Kihara","doi":"10.1007/s12035-025-05020-2","DOIUrl":"10.1007/s12035-025-05020-2","url":null,"abstract":"<p><p>Hippocampal interneurons (INs) play a fundamental role in regulating neural oscillations, modulating excitatory circuits, and shaping spatial representation. While historically overshadowed by excitatory pyramidal cells in spatial coding research, recent advances have demonstrated that inhibitory INs not only coordinate network dynamics but also contribute directly to spatial information processing. This review aims to provide a novel integrative perspective on how distinct IN subtypes participate in spatial coding and how their dysfunction contributes to cognitive deficits in neurological disorders such as epilepsy, Alzheimer's disease (AD), traumatic brain injury (TBI), and cerebral hypoxia-ischemia. We synthesize recent findings demonstrating that different IN classes-including parvalbumin (PV)-, somatostatin (SST)-, cholecystokinin (CCK)-, and calretinin (CR)-expressing neurons-exhibit spatially selective activity, challenging traditional views of spatial representation, and influence memory consolidation through network-level interactions. By leveraging cutting-edge techniques such as in vivo calcium imaging and optogenetics, new evidence suggests that INs encode spatial information with a level of specificity previously attributed only to pyramidal cells. Furthermore, we investigate the impact of inhibitory circuit dysfunction in neurological disorders, examining how disruptions in interneuronal activity lead to impaired theta-gamma coupling, altered sharp wave ripples, and destabilized place cell representations, ultimately resulting in spatial memory deficits. This review advances the field by shifting the focus from pyramidal-centered models to a more nuanced understanding of the hippocampal network, emphasizing the active role of INs in spatial coding. By highlighting the translational potential of targeting inhibitory circuits for therapeutic interventions, we propose novel strategies for restoring hippocampal network function in neurological conditions. Readers will gain a comprehensive understanding of the emerging role of INs in spatial representation and the critical implications of their dysfunction, paving the way for future research on interneuron-targeted treatments for cognitive disorders.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14777-14800"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144111451","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":"Intervention Role of APOE in CNS Diseases: APOE Actions and APOE Neurogenesis Capability.","authors":"Wenhua Li, Suya Ma, Min Li","doi":"10.1007/s12035-025-05028-8","DOIUrl":"10.1007/s12035-025-05028-8","url":null,"abstract":"<p><p>Neurogenesis is a biological process in which new neurons are generated from neural stem cells (NSCs) in specific neural niches in the brain. Impaired neurogenesis, characterized by the progressive loss of neurons, leads to cognitive and motor disabilities and is a hallmark of central nervous system (CNS) diseases. Conversely, enhancing neurogenesis has been shown to alleviate the symptoms of CNS diseases. Apolipoprotein E (APOE) is a protein that plays various biological roles in CNS diseases. Emerging research indicates that APOE is involved in adult neurogenesis, which is crucial for maintaining the neural progenitor pool in the dentate gyrus (DG) and synaptic activity. Therefore, APOE could be a therapeutic target for promoting neurogenesis in the treatment and intervention of CNS diseases. In this context, we present a comprehensive overview of the clinical evidence supporting the role of APOE in CNS diseases on the basis of a meta-analysis. We also discuss the neurogenic potential of APOE, which has significant implications not only for understanding the biological underpinnings of neurological diseases but also for developing novel treatment strategies for CNS diseases.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14811-14833"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144120190","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 Double-Edged Effect of Connexins and Pannexins of Glial Cells in Central and Peripheral Nervous System After Nerve Injury.","authors":"Yue-Yan Cen, Xin-Lin Gao, Yu-Heng Feng, Cheng Zhou, Chun-Jie Li, Fei Liu, Jie-Fei Shen, Yan-Yan Zhang","doi":"10.1007/s12035-025-04991-6","DOIUrl":"10.1007/s12035-025-04991-6","url":null,"abstract":"<p><p>Glial cells play pivotal roles in homeostatic regulation and driving reactive pathologic changes after nerve injury. Connexins (Cxs) and pannexins (Panxs) have emerged as seminal proteins implicated in cell-cell communication, exerting a profound impact on the response processes of glial cell activation, proliferation, protein synthesis and secretion, as well as apoptosis following nerve injury. These influences are mediated through various forms, including protein monomers, hemichannel (HC), and gap junction (GJ), mainly by regulating intercellular or intracellular signaling pathways. Multiple Cx and Panx isoforms have been detected in central nervous system (CNS) or peripheral nervous system (PNS). Each isoform exhibits distinct cellular and subcellular localization, and the differential regulation and functional roles of various protein isoforms are observed post-injury. The quantitative and functional alterations of the same protein isoform in different studies remain inconsistent, attributable to factors such as the predominant mode of protein polymerization, the specific injury model, and the injury site. Similarly, the same protein isoforms have different roles in regulating the response processes after nerve injury, thus exerting a double-edged sword effect. This review describes the regulatory mechanisms and bidirectional effects of Cxs and Panxs. Additionally, it surveys the current status of research and application of drugs as therapeutic targets for neuropathic injuries. We summarize comprehensive and up-to-date information on these proteins in the glial cell response to nerve injury, providing new perspectives for future mechanistic exploration and development of targeted therapeutic approaches.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14474-14518"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144035536","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":"REST/NRSF Regulation of Epilepsy and Cognitive Impairment: Mechanisms and EEG Correlations.","authors":"Liang OUyang, Xiao-Xuan Li, Bing Li","doi":"10.1007/s12035-025-05138-3","DOIUrl":"10.1007/s12035-025-05138-3","url":null,"abstract":"<p><p>This study aimed to investigate the relationship between REST/NRSF and cognitive impairment in epilepsy, focusing on EEG alterations and serum REST/NRSF levels as potential biomarkers. Additionally, the study explored how REST/NRSF regulation in the hippocampus affects epileptic activity and cognitive function through the modulation of Kv7.2/7.3 potassium channels. We studied 50 epilepsy patients (25 with cognitive impairment, 25 without) and 40 healthy controls. High-density EEG was used to assess brain activity across various frequency bands. Serum REST/NRSF levels were measured by ELISA and correlated with cognitive performance (MoCA). ROC analysis and logistic regression assessed the predictive value of EEG and REST/NRSF for cognitive dysfunction. In animal models, KA-induced epileptic mice were used to study REST/NRSF expression and its effect on Kv7.2/7.3 channels through Western blotting and qRT-PCR. The δ relative power and DTABR in the left frontoparietal, left frontotemporal, and left temporal regions of the epilepsy cognitive impairment group were significantly higher than those of the non-cognitive impairment and control groups (P < 0.05); conversely, the α relative power in the same regions was significantly lower (P < 0.05). Serum REST/NRSF levels were significantly higher in the cognitive impairment group and negatively correlated with cognitive function (P < 0.05). ROC curve analysis revealed high predictive value for δ and α frequency band power and serum REST/NRSF levels for cognitive dysfunction in epilepsy (AUC > 0.8). In KA model mice, REST/NRSF protein levels were significantly elevated in the hippocampal CA1 region, while Kv7.2/7.3 expression was reduced. Knockdown of REST/NRSF in the hippocampus resulted in reduced seizure severity, while overexpression of REST/NRSF exacerbated seizures. This study demonstrates that cognitive impairment in epilepsy is linked to changes in EEG power spectra and elevated serum REST/NRSF levels. These findings suggest that REST/NRSF plays a role in regulating both epileptic activity and cognitive dysfunction, potentially through modulation of Kv7.2/7.3 potassium channels. These results highlight REST/NRSF as a promising biomarker and therapeutic target for cognitive impairment in epilepsy.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14176-14195"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144659674","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":"Calcium Signaling in Astrocytes and Its Role in the Central Nervous System Injury.","authors":"Xinyue Li, Lu Ding, Hong Nie, David Y B Deng","doi":"10.1007/s12035-025-05055-5","DOIUrl":"10.1007/s12035-025-05055-5","url":null,"abstract":"<p><p>Astrocytes are the most abundant glial cells in the central nervous system (CNS). Due to their extensive processes, they can interconnect with many neighboring cells and play critical roles in regulating synaptic plasticity, integrating neuronal signals, and maintaining the stability of the extracellular environment. These functions are largely dependent on calcium (Ca²⁺) signaling. In light of these considerations, the powerful functions of Ca²⁺ signaling in astrocytes have been actively studied in recent years. This review summarizes the mechanisms related to Ca²⁺ waves in astrocytes as well as their physiological and pathological functions mediated by various calcium signaling, the characteristics of calcium waves, and the role of Ca²⁺ in astrocytes in the CNS injuries of spinal cord injury (SCI) and traumatic brain injury (TBI) recently. However, inhibited L-type voltage-gated Ca²⁺ channels (LTCCs) activity and reduced Ca²⁺ concentration result in an opposite phenomenon that promoting or reducing astrogliosis. This highlights the importance of focusing not only on Ca²⁺ concentration but also on the downstream signaling pathways initiated by Ca²⁺. Therefore, we summarize diverse signaling pathways in various physiological and pathological contexts.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14947-14965"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151256","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 Notch Signaling Pathway: A Potential Target for Mental Disorders.","authors":"Qian Zhang, Jingxuan Zheng, Hongqin Sun, Jishan Zheng, Yunyan Ma, Qinglu Ji, Dengwang Chen, Zhengzhen Tang, Jidong Zhang, Yuqi He, Tao Song","doi":"10.1007/s12035-025-05034-w","DOIUrl":"10.1007/s12035-025-05034-w","url":null,"abstract":"<p><p>The highly conserved Notch signaling pathway plays a critical role in cell fate determination during metazoan development through cell-to-cell communication. The classical pathway consists of Notch receptors, ligands, intracellular effectors, DNA-binding proteins, and other regulatory molecules. Recent research has highlighted its involvement in the pathogenesis of several diseases. In autism, bipolar disorder, and schizophrenia, the Notch signaling pathway is implicated in key processes such as neuronal development and synaptic plasticity. Furthermore, it has been shown to play significant roles in other mental health conditions, including anxiety, depression, post-traumatic stress disorder, and neurocognitive disorders. However, the precise mechanisms underlying the contribution of Notch to these conditions remain poorly understood. This review examines the current understanding of the Notch signaling pathway in mental disorders, highlighting its role in their pathophysiology and summarizing therapeutic strategies aimed at modulating this pathway to improve mental health outcomes.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14717-14733"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079128","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 Cooperation of Neurogranin with Calmodulin Promotes the Treatment of Aging-Related Diseases via Regular Exercise.","authors":"Hosniyeh Rajavand, Vahideh Zalouli, Zeinab Nematollahi, Farshid Fathy-Karkaragh, Elham Karimigharighi, Farzad Jafarizadeh, Amirhossein Rabiei Rad","doi":"10.1007/s12035-025-04959-6","DOIUrl":"10.1007/s12035-025-04959-6","url":null,"abstract":"<p><p>Research has demonstrated that engaging in regular exercise has the potential to enhance cognitive function, promote neuroplasticity, and mitigate the likelihood of experiencing cognitive decline. The underlying mechanisms responsible for these effects are intricate and encompass various pathways, including the interaction between neurogranin and calmodulin. The activation of calcium signaling pathways is a significant mechanism through which regular exercise facilitates the treatment of age-related diseases. The activation of neurogranin and calmodulin induced by exercise can provide protection against neurodegeneration by promoting neuronal survival, mitigating oxidative stress, and improving mitochondrial function through the regulation of calcium homeostasis and energy metabolism. In addition, there is evidence suggesting that engaging in regular exercise can lead to an upregulation of neurotrophic factors, specifically brain-derived neurotrophic factor (BDNF). These factors are crucial for the survival of neurons, the plasticity of synapses, and overall cognitive function. Researchers have discovered the involvement of neurogranin in the regulation of BDNF signaling, underscoring its significance in exercise-induced neuroprotection and cognitive enhancement. The current work offers valuable insights into how neurogranin/calmodulin cooperation, facilitated by regular exercise, promotes the treatment of aging-related diseases. The results suggest that regular exercise could enhance memory, learning, synaptic plasticity, and resilience to neurological damage; promote recovery after brain injury; and treat aging-related disorders such as Alzheimer's disease.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14387-14406"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144011705","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":"Peripheral Blood Mononuclear Cell Mitochondrial Bioenergetics Is Impaired in De Novo Parkinson's Disease.","authors":"Samantha Varada, Amber L Prasad, Brenna M Lobb, Lee E Neilson, Jonathan E Elliott, Miranda M Lim, Barbara H Brumbach, Joseph F Quinn, Nora E Gray","doi":"10.1007/s12035-025-05224-6","DOIUrl":"10.1007/s12035-025-05224-6","url":null,"abstract":"<p><p>Mitochondrial dysfunction is increasingly recognized as a key driver of pathology in patients with Parkinson's disease (PD). Peripheral blood mononuclear cells (PBMCs) have emerged as an accessible way to characterize mitochondrial function in PD. The aim of this study was to conduct a preliminary evaluation of the clinical relevance of PBMC mitochondrial function as a biomarker in early PD. PBMC mitochondrial bioenergetics were measured using the Seahorse XF platform in individuals with de novo, untreated PD (n = 13) and compared to age- and sex-matched healthy controls (n = 15). Correlations between mitochondrial endpoints and clinical outcomes were assessed in the PD group. Basal and ATP-linked respiration were elevated in the PD group (p = 0.002, p = 0.004), while spare capacity, or the cell's ability to handle an unexpected energetic stress, was decreased (p = 0.045), relative to controls. Notably, the variability within basal respiratory measurements was markedly increased in the PD group compared to controls (p = 0.002). Further analyses revealed significant correlations between spare capacity and clinical motor function scores within the PD group. These findings support the potential of PBMC bioenergetics as a biomarker for early-stage PD as well as disease progression.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14221-14226"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668010","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 Potential Protective Effects of Intermittent Fasting Against Radiation-Induced Brain Damage in a Rat Model: Suggested Involvement of IRS-1/PI3 K/AKT and BDNF/TrkB Signaling Pathways.","authors":"Eman F S Taha, Hebatallah E Mohamed, Lobna M Anees, Hayam Mostafa, Eman S Eldin","doi":"10.1007/s12035-025-05059-1","DOIUrl":"10.1007/s12035-025-05059-1","url":null,"abstract":"<p><p>Fasting has emerged as a promising therapeutic strategy for neurological disorders, offering protection against insults such as ionizing radiation (IR), which can cause irreversible brain damage. Intermittent fasting (IF), including alternate-day fasting (ADF) and time-restricted feeding (TRF), is being explored for its neuroprotective effects with potential involvement of key signaling pathways such as IRS-1/PI3K/AKT and BDNF/TrkB. Thirty-six male Wistar albino rats were randomly divided into six groups: normal feeding (NF, ad libitum feeding), ADF, TRF (6-h feeding window), NF plus radiation (NF-irradiated, 20-Gy cranial exposure), ADF plus radiation (ADF-irradiated), and TRF plus radiation (TRF-irradiated). Oxidative stress markers, antioxidant enzymes, liver and kidney function parameters, and gene/protein expression levels (IRS1, AKT1, PI3K, GFAP, 8-OHdG, BDNF, TrkB) were evaluated using enzyme-linked immunosorbent assay (ELISA) and RT-PCR, complemented by histopathological analysis. IR significantly impaired antioxidant defenses (GSH, GST, CAT), suppressed IRS-1/PI3K/AKT and BDNF/TrkB signaling, and elevated oxidative damage markers (MDA, ROS, 8-OHdG), inflammation (GFAP), and markers of organ dysfunction (ALT, AST, GGT, urea, creatinine). Both IF regimens mitigated these effects; however, TRF demonstrated greater efficacy than ADF. TRF more effectively reduced oxidative stress, improved antioxidant enzyme activity, and more robustly restored metabolic and neurotrophic signaling pathways. Both ADF and TRF provided neuroprotection against radiation-induced brain injury, but TRF exhibited superior outcomes in reducing oxidative stress and preserving neuronal integrity. These findings highlight TRF as a potentially more effective dietary strategy for mitigating radiation-induced neurotoxicity, with possible contributions from the modulation of IRS-1/PI3K/AKT and BDNF/TrkB pathways.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"13807-13826"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511218/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}