Frontiers in Molecular Neuroscience最新文献

{"title":"Integrative genomic analysis identifies key target genes and candidate drugs for spinal stenosis.","authors":"Demeng Xia, Yongjie Chen, Rui Wu, Yifan Tang, Yanqing Sun, Xiongsheng Chen","doi":"10.3389/fnmol.2026.1767263","DOIUrl":"https://doi.org/10.3389/fnmol.2026.1767263","url":null,"abstract":"<p><strong>Background: </strong>Spinal stenosis is a common pathological condition characterized by the narrowing of the spinal canal, contributing to substantial morbidity and imposing a significant socioeconomic burden. Despite its clinical importance, the genetic drivers and cellular mechanisms driving its progression remain inadequately understood, necessitating integrative approaches to identify therapeutic targets.</p><p><strong>Methods: </strong>This study employed an integrative multi-omics strategy. Initially, summary-data-based Mendelian randomization was conducted using cis-expression quantitative trait loci data from 19,960 genes alongside spinal stenosis genome-wide association study data. Gene-gene interaction networks and colocalization analyses further refined candidate genes. Additionally, single-cell RNA sequencing of spinal tissues was performed to assess cellular enrichment, and molecular docking was employed to screened FDA-approved drugs against prioritized targets. Immunohistochemistry (IHC), Western blot (WB), and quantitative real-time PCR (qRT-PCR) were conducted using tissue samples and primary cells to validate the bioinformatics analysis results.</p><p><strong>Results: </strong>SMR analysis identified 45 candidate target genes, which were further narrowed to three key genes including KAT5, TET2, and TAF10 through gene-gene interaction analysis and colocalization. Single-cell RNA sequencing revealed that these genes were predominantly enriched in chondrocytes and monocytes, implicating cellular cross-talk via the TGF-β1- (TGF-βR1 ++ TGF-βR2) pathway, a driver of fibrosis and ossification. Molecular docking identified six high-affinity compounds: Balsalazide and Eltrombopag for KAT5, Magnesium Citrate and Ferric Citrate for TET2, and Piracetam and Deferiprone for TAF10. The expression level of KAT5 and TET10 were both consistent with our SMR analysis in both tissues and primary cells.</p><p><strong>Conclusion: </strong>These findings elucidate novel genetic and cellular mechanisms underlying spinal stenosis, highlighting the role of TGF-β pathway in disease progression. The identified compounds offer promising therapeutic interventions, bridging genomic discoveries to clinical applications and paving the way for targeted treatment strategies.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1767263"},"PeriodicalIF":3.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13079337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147698299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic pain, fatigue, and emotional distress in female <i>FMR1</i> premutation carriers.","authors":"Dragana Protic, Maja Stojkovic, Randi Hagerman, Danijela Bascarevic, Jovana Ogrizovic, Sanja Dimitrijevic, Jovan Pesovic, Dusanka Savic-Pavicevic, Dejan Budimirovic","doi":"10.3389/fnmol.2026.1741854","DOIUrl":"https://doi.org/10.3389/fnmol.2026.1741854","url":null,"abstract":"<p><strong>Introduction: </strong>Carriers of the <i>FMR1</i> gene premutation (PM) are at increased risk for Fragile X-associated PM Conditions (FXPAC). Some clinically significant symptoms can be further classified as Fragile X-associated Neuropsychiatric Disorders (FXAND). Many FXAND-related cases may go underrated and untreated. This study aimed to investigate the rates of FXAND-related symptoms among female PM carriers.</p><p><strong>Methods: </strong>The study was conducted at the Belgrade Fragile X Clinic on a clinical sample of 35 women with the PM and 35 controls using an adapted version of the Symptom Impact Questionnaire and the Fatigue Assessment Scale. The survey was designed to collect data on FXAND symptoms, including chronic pain, fatigue, anxiety, and depressive symptoms. Each symptom was self-rated by participants on a scale from 0 to 10. Data were analyzed using appropriate statistical methods.</p><p><strong>Results: </strong>Women with the PM (mean age: 44.51 ± 12.90 y.; 90.51 ± 22.04 CGG repeats) had statistically significant higher frequency and severity of chronic pain (<i>p</i> = 0.03; <i>p</i> = 0.02) and fatigue (<i>p</i> = 0.001 for both) in contrast to age-matched controls. Although the prevalence of anxiety symptoms was not significantly different between groups, the severity of anxiety symptoms were significantly higher in the PM group (<i>p</i> < 0.001), and was positively correlated with chronic fatigue (<i>p</i> = 0.003 vs. <i>p</i> = 0.27 in controls). Depressive symptom frequency and severity did not differ between groups (<i>p</i> = 0.47; <i>p</i> = 0.55), but there were a significant positive correlation between anxiety and depressive symptoms in the PM group (<i>p</i> = 0.003). Depressive symptoms were also positively correlated with chronic fatigue in the PM group (<i>p</i> = 0.02), but not in controls (<i>p</i> = 0.58). Compared to controls, PM carriers reported more frequently lower energy, poorer sleep, greater memory issues, cognitive difficulties, balance problems, and increased sensory sensitivity (<i>p</i> ≤ 0.001, all).</p><p><strong>Conclusion: </strong>Female PM carriers experience significantly higher frequency and severity of FXAND-related symptoms. Our findings of an association between fatigue, anxiety, and depressive symptoms highlight the need for comprehensive screening and underscore the importance of recognizing and treating individuals with FXAND.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1741854"},"PeriodicalIF":3.8,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13057454/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CNP-induced cGMP signaling reduces growth cone stiffness and Ca²⁺ levels in embryonic DRG neurons.","authors":"Aylin Balmes, Hannes Schmidt, Stefanie Peters, Selin Kenet, Adelina Botezatu, Lai Wen, Alexandra Böttcher, Peter M Benz, Robert Feil, Tilman E Schäffer","doi":"10.3389/fnmol.2026.1769175","DOIUrl":"https://doi.org/10.3389/fnmol.2026.1769175","url":null,"abstract":"<p><p>A cyclic guanosine monophosphate (cGMP) signaling pathway composed of the extracellular ligand C-type natriuretic peptide (CNP), the transmembrane natriuretic peptide receptor 2 (Npr2), and the cGMP-dependent protein kinase I (cGKI) regulates axon bifurcation of embryonic dorsal root ganglion (DRG) neurons in mice. Despite the importance of this process for the development of neuronal connectivity, the underlying mechanisms are only partially understood. Axon bifurcation requires an orchestrated rearrangement of the cytoskeleton in growth cones, the highly motile structures at axon tips. In this study, we explored the effects of cGMP signaling on growth cones in fixed and living DRG explant cultures obtained from mouse embryos. The cytoskeletal organization and stiffness of growth cones was examined by fluorescence microscopy and scanning ion conductance microscopy (SICM). Activation of cGMP signaling by CNP or the membrane-permeable cGMP analog 8-Bromo-cGMP reduced growth cone and axon shaft stiffness. Experiments with DRG neurons from Npr2 knockout (KO) mice confirmed that the anti-stiffness effect of CNP was Npr2-dependent. Pharmacological disruption of the cytoskeleton revealed that growth cone stiffness was determined by F-actin content. Activation of cGMP signaling reduced F-actin content in growth cones. Next, we studied the mechanism of cGMP-mediated cytoskeletal remodeling in growth cones. Genetic deletion of vasodilator-stimulated phosphoprotein (Vasp), a phosphorylation target of cGKI that regulates actin polymerization, did not impair cGMP-induced reduction of growth cone and axon shaft stiffness <i>in vitro</i> and axon bifurcation <i>in vivo</i>. Since growth cone dynamics is also regulated by the intracellular Ca²⁺ concentration, we performed simultaneous imaging of cGMP and Ca²⁺ in living growth cones. CNP-induced cGMP elevations suppressed ATP-induced Ca²⁺ transients in wild-type growth cones, but not in cGKI-deficient growth cones. In summary, this study indicates that the CNP-Npr2-cGMP-cGKI axis in DRG neurons controls Ca²⁺ signaling, remodeling of the actin cytoskeleton, and growth cone mechanics. Thereby, it might contribute to regulating axonal branching.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1769175"},"PeriodicalIF":3.8,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13055628/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147638625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated genetic analysis reveals synaptic m⁶A enrichment in high-risk autism genes.","authors":"Shreya Doijad, Divyadharshini Sakthivel, Naveen Kumar Chandappa Gowda","doi":"10.3389/fnmol.2026.1767983","DOIUrl":"https://doi.org/10.3389/fnmol.2026.1767983","url":null,"abstract":"<p><p>Autism Spectrum Disorder (ASD), a complex neurodevelopmental condition, is characterised by reduced social and emotional expression and repetitive patterns of behaviour. The clinical observations of defects in brain development and disrupted connectivity in ASD correlate with the perturbations at the neuronal and molecular levels. While the underlying genetic basis has been extensively studied, understanding the epigenetic and epitranscriptomic regulation has only begun to unravel in the past two decades. This work aims to link the ASD clinical phenotypes to the molecular dysfunction, specifically highlighting one of the crucial mRNA modifications, N6-methyladenosine (m⁶A). During neuronal development, m⁶A, a key post-transcriptional regulator, dynamically modulates mRNA translation at synapses and is essential for maintaining synaptic plasticity. However, the mechanisms by which m⁶A operates at synapses in the context of ASD are poorly understood. Our work establishes connections across neuronal developmental timelines to m⁶A regulation and discusses the possibility of how this dysregulation may underlie the development of synaptopathies observed in ASD. By integrating previously published m⁶A-seq and CLIP-seq data with the SFARI gene database, we found that 41.59% (515 of 1,238 genes) of ASD risk genes are m⁶A-enriched. Specifically, we found 28 syndromic genes overlapping with the Synaptic m⁶A Epitranscriptome (SME). Here, we also shed light on the importance of m⁶A readers, with a focus on FMRP and YTHDF1 and their regulation at the synapse. Altogether, we suggest a model in which m⁶A-mediated post-transcriptional regulation influences ASD-related synaptic dysfunction.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1767983"},"PeriodicalIF":3.8,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13047897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147622686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Neuroglycobiology.","authors":"Cyril Hanus, Robert G Mealer, Liqin Zhao, Thomas S Klarić","doi":"10.3389/fnmol.2026.1814339","DOIUrl":"https://doi.org/10.3389/fnmol.2026.1814339","url":null,"abstract":"","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1814339"},"PeriodicalIF":3.8,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13038605/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147608764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TDP-43 related amyotrophic lateral sclerosis-frontotemporal dementia and links to the DNA damage response: a systematic review and narrative synthesis.","authors":"Seham Almalki, Mohamed Salama, Matthew J Taylor, Zubair Ahmed, Richard I Tuxworth","doi":"10.3389/fnmol.2026.1671909","DOIUrl":"https://doi.org/10.3389/fnmol.2026.1671909","url":null,"abstract":"<p><p>Mislocalization and aggregation of the DNA/RNA binding protein, TDP-43, is seen in most cases of amyotrophic lateral sclerosis-frontotemporal dementia (ALS-FTD). Accumulating DNA damage in neurons is also a common feature of ALS-FTD. TDP-43 has several characterized roles in the regulation of the DNA damage response (DDR). This review systematically explored the relationship between TDP-43, DNA damage and the DNA damage response in various models of ALS-FTD, facilitating comparison of findings between studies using similar models. Twelve peer-reviewed papers, covering eight TDP-43 mutations out of nearly 40, were reviewed and five experimental models included: cell lines, patient-derived iPS cells, organoids, and rodent models, plus post-mortem cortex and spinal cord tissue from ALS-FTD patients. Across the studies and models, depletion of TDP-43 or ALS-linked mutations consistently increased genomic instability. Q331K-expressing cells showed a 2-3-fold reduction in DNA repair activity and a 4-6-fold increase in DDR activation, while <i>TDP-43</i>-depleted cells showed a 20-fold rise in double strand breaks. TDP-43 normally binds to damaged chromatin, participates in early DDR signaling and scaffolds core DNA damage repair factors, including Ku70, XRCC4 and DNA ligase 4. This systematic review and narrative synthesis sheds light on mechanisms that explain how TDP-43 dysfunction impairs genome maintenance. When TDP-43 is mislocalized, mutated or aggregated, these interactions are disrupted, resulting in impaired DNA repair. DNA damage is also caused by increasing R-loops, dysregulation of mismatch repair gene transcription, and sequestering of repair proteins into cytoplasmic inclusions. Upstream DNA damage can further drive TDP-43 mislocalisation, creating a feed-forward loop. Given the ubiquity of TDP-43 pathology across neurodegenerative diseases, targeting the DDR mechanisms affected by TDP-43 may offer new therapeutic opportunities.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1671909"},"PeriodicalIF":3.8,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13036212/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147591603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glycine transport inhibitors for the treatment of chronic pain conditions: the time is ripe for clinical evaluation!","authors":"Volker Eulenburg, Christopher L Cioffi, Anutosh Roy, Robert J Vandenberg","doi":"10.3389/fnmol.2026.1793163","DOIUrl":"https://doi.org/10.3389/fnmol.2026.1793163","url":null,"abstract":"","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1793163"},"PeriodicalIF":3.8,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13036110/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147591639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction: Selected thiadiazine-thione derivatives attenuate neuroinflammation in chronic constriction injury induced neuropathy.","authors":"","doi":"10.3389/fnmol.2026.1827289","DOIUrl":"https://doi.org/10.3389/fnmol.2026.1827289","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3389/fnmol.2021.728128.].</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1827289"},"PeriodicalIF":3.8,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13036976/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147591675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polyclonal glycine receptor aAbs: a challenge for personalized epitope characterization.","authors":"Anna-Lena Wiessler, Inken Stahl, Natascha Schaefer, Vera Rauschenberger, Ivan Talucci, Hans M Maric, Betül Baykan, Erdem Tüzün, Claudia Sommer, Carmen Villmann","doi":"10.3389/fnmol.2026.1747209","DOIUrl":"https://doi.org/10.3389/fnmol.2026.1747209","url":null,"abstract":"<p><strong>Introduction: </strong>Patients with glycine receptor (GlyR) aAbs suffer from various diseases, including stiff-person syndrome (SPS), and currently, no cure exists. Several treatment options exist; however, these treatment options lack specificity. To date, only one common epitope has been mapped for GlyR aAbs in the far N-terminal region of the GlyRα1 subunit. However, some patient sera also bind GlyRα2, GlyRα3, or GlyRβ. Therefore, more than one common epitope may exist. Unraveling these epitopes will help generate more specific treatment approaches.</p><p><strong>Methods: </strong>Here, we constructed GlyRa1 and GlyRa3 variants by site-directed mutagenesis using amino acid differences between these two subunits within their extracellular domains. Peptide microarrays, which have shown that an epitope including the binding site of a commercial pan-a antibody (⁹⁶PDLFFANEKS¹⁰⁵) and its surrounding residues is highly relevant for aAb binding, were utilized to identify additional residues important for aAb binding. Two overlapping peptides (⁹³LWKPDLFFANEKSAN¹⁰⁷ and ⁹⁸LFFANEKSANFHDVT¹¹²) were used for aAb neutralization in cell-based assays.</p><p><strong>Results: </strong>The GlyRa1 and GlyRa3 variants helped to identify which amino acid sequences in the extracellular domain of GlyRs represent additional aAb epitopes or are involved in aAb binding. Using both generated peptides for aAb neutralization with a patient serum containing GlyRb aAbs that bind specifically to this region ⁹⁶PDLFFANEKSANFHDV¹¹¹, successful neutralization was demonstrated. In contrast, when using patient sera that reliably target the extracellular domain including ⁹⁶PDLFFANEKS¹⁰⁵ of the GlyRa subunits, the overlapping peptides reduced aAb binding but failed to fully neutralize the aAbs.</p><p><strong>Discussion: </strong>In conclusion, our data demonstrate that GlyR aAbs are polyclonal or bind to structural epitopes. These results define single residues important for aAb binding and help explain why no further common aAb binding site has been identified so far. Hence, patient-specific pattern for GlyR aAbs exist, emphasizing the importance of epitope characterization as basis for future therapeutic testing or even complete neutralization of the aAbs.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1747209"},"PeriodicalIF":3.8,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13036184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147591690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mentorship, memory, and honor: Rita Levi-Montalcini's legacy and the role of academic recognition in promoting women in science.","authors":"Léa Sun, Guila Delouya, Daniel Taussky","doi":"10.3389/fnmol.2026.1775988","DOIUrl":"10.3389/fnmol.2026.1775988","url":null,"abstract":"<p><p>The contemporary vignette highlights how the mentorship model exemplified by Rita Levi-Montalcini continues to foster scientific identity, confidence, and career progression, especially among women and minorities facing systemic barriers. Through a mixed-methods narrative approach, combining historical-biographical review, qualitative analysis of a contemporary mentee vignette, and bibliometric insights. Levi-Montalcini's own experience under Giuseppe Levi's mentorship demonstrated the critical psychosocial and instrumental support necessary to develop resilience and scientific rigor. This research highlights how mentorship by Giuseppe Levi shaped Levi-Montalcini's scientific rigor and resilience, contributing to her Nobel Prize-winning discoveries. Similarly, modern mentorship and institutional honors serve to counteract stereotype threats and enhance retention by providing recognition through awards and leadership roles, reflecting Levi-Montalcini's legacy of transforming private perseverance into a public authority. This study underscores that structured mentorship programs and transparent recognition systems, inspired by Levi-Montalcini's trajectory, are essential for universities to promote inclusive excellence and empower emerging women scientists in STEM (Science, Technology, Engineering, and Mathematics) fields.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1775988"},"PeriodicalIF":3.8,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13021874/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147573650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}