Cellular and Molecular Neurobiology最新文献

{"title":"Protein Arginine Methyltransferases from Regulatory Function to Clinical Implication in Central Nervous System.","authors":"Bin Xie, Jing Yu, Chao Chen, Ting Shen","doi":"10.1007/s10571-025-01546-0","DOIUrl":"10.1007/s10571-025-01546-0","url":null,"abstract":"<p><p>Arginine methylation, catalyzed by protein arginine methyltransferases (PRMTs), is a regulatory key mechanism involved in various cellular processes such as gene expression, RNA processing, DNA damage repair. Increasing evidence highlights the crucial role of PRMTs in human diseases, including cancer, cardiovascular and metabolic diseases. Here, this review focuses on the latest findings regarding PRMTs in the central nervous system (CNS), emphasizing their regulatory roles in neural stem cells, neurons, and glial cells. Additionally, we examine the connection between PRMTs dysregulation and neurological diseases affecting the CNS, including brain tumors, neurodegenerative diseases, and neurodevelopmental disorders. Therefore, this review aims to deepen our understanding of PRMTs-mediated arginine methylation in CNS and open avenues for developing novel therapeutic strategies for neurological diseases.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"41"},"PeriodicalIF":3.6,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078925/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synergistic Effects of Olfactory Ecto-Mesenchymal Stem Cell Supernatant and Ellagic Acid on Demyelination and Glial Modulation in a Chronic Multiple Sclerosis Model.","authors":"Fatemeh Tahmasebi, Elmira Roshani Asl, Faezeh Faghihi, Nadia Bolandi, Shirin Barati","doi":"10.1007/s10571-025-01558-w","DOIUrl":"https://doi.org/10.1007/s10571-025-01558-w","url":null,"abstract":"<p><p>Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system. Stem cells as a source of neurotrophic factors and ellagic acid (EA) as an antioxidant reduce the progression of neurodegenerative diseases. In this study, we evaluated the effect of olfactory ecto-mesenchymal stem cell (EMSC) supernatant and EA on A1 astrocytes, M1 microglia, and demyelination in cuprizone model. To induce the chronic demyelination model, mice received a diet containing 0.2% cuprizone/kg of food for 12 weeks. EMSC supernatant was injected into the lateral ventricle of mice. EA was administered intraperitoneally daily at a dose of 80 mg/kg body weight for two weeks. Two weeks after injection, immunohistochemistry was performed to detect the presence of astrocytes (GFAP), microglia/macrophages (Iba-1), and oligodendrocytes (Olig2). The level of gene expression of EMSC (TGF-β and BDNF), astrocytes (C3 and GBP2) and microglia (iNOS, TNF-α and IL-6) was evaluated by qRT-PCR method. The results showed that injection of EMSC and EA increased the expression of TGF-β and BDNF genes as trophic factors. LFB images showed that supernatant and EA significantly improved remyelination, which was accompanied by an increase in oligodendrocyte population. The astrocyte population increased in the cuprizone group, while it decreased after supernatant and EA administration. The supernatant and EA decreased microglia after cuprizone induction. The qRT-PCR showed neurotoxic genes of A1 and M1 decreased after supernatant and EA administration. Here, we demonstrate that EMSC supernatant and EA could improve demyelination in neurodegenerative diseases such as MS by reducing microgliosis and astrocytosis in addition to increasing myelination.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"40"},"PeriodicalIF":3.6,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12048376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143987087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurofilament Light Chain Correlates with Stroke Severity and Clinical Outcome in Acute Cerebrovascular Stroke Patients.","authors":"Abeer Abdelhady Tony, Emad Farah Mohammad Kholef, Dalia B Elgendy, Ahmed Shoyb","doi":"10.1007/s10571-025-01552-2","DOIUrl":"https://doi.org/10.1007/s10571-025-01552-2","url":null,"abstract":"<p><p>Serum neurofilament light chain (sNfL) is a marker of injury in many chronic neurological Disorders. We assessed NF-L in patients with acute stroke (ischemic or hemorrhagic) and healthy controls and clarified its association with the stroke severity, etiology, and functional outcome. This case-control study was conducted on 85 patients with first-ever acute stroke (ischemic or hemorrhagic) and 85 control subjects. Participants were subjected to through neurological history and examination. Brain imaging was performed after hospital admission. Blood tests were drawn for assessment of serum neurofilament (sNfL) levels at the first day of admission. Compared to healthy controls, our stroke patients either Ischemic or hemorrhagic had increased sNfL levels. Despite not being statistically different, ischemic stroke patients had greater levels than hemorrhagic stroke patients. Higher sNfL levels were associated with higher NIHSS scores and mRS at admission. In patients with ICH, a correlation was observed between sNfL and hematoma volume, hemorrhage location, ventricular extension and mRS. Moreover, an association of sNfL with Ischemic stroke due to large artery atherosclerosis was reported. In the absence of additional predictive variables like age and sex, it may be possible to quantify sNfL in acute plasma samples as a potential indicator of functional prognosis in patients with ischemic and hemorrhagic strokes. To validate sNfL as a biomarker for acute stroke, however, further research involving a larger number of patients is necessary.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"39"},"PeriodicalIF":3.6,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12044141/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143985701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating Biomarkers to Predict Post-Operative Cognitive Decline in Patients Undergoing Coronary Artery Bypass Grafting.","authors":"Vitale Miceli, Emanuele Lo Gerfo, Giovanna Russelli, Matteo Bulati, Gioacchin Iannolo, Rosaria Tinnirello, Maura Cimino, Luciano Saso, Federica Avorio, Vincenzina Lo Re","doi":"10.1007/s10571-025-01553-1","DOIUrl":"https://doi.org/10.1007/s10571-025-01553-1","url":null,"abstract":"<p><p>Post-operative cognitive decline (POCD) is characterized by impairments in cognitive functions. Coronary artery bypass grafting (CABG) is associated with a high risk of POCD due to its impact on neuroinflammation and oxidative stress. In this study, we investigated the dynamics of neurotrophic, inflammatory, and oxidative stress markers in a cohort of post-CABG patients to identify potential biomarkers for POCD. Blood samples were collected at baseline (immediately post-surgery) and at 3-month follow-up. Expression levels of NRF2 and other regulators of oxidative stress (GST, GSS, HMOX1, CAT, HSP27, and LOX-1), inflammatory mediators (IL-6, IP-10, and NFκB), and neuroprotective factor (BDNF) were analyzed. Cognitive assessments were performed using RBANS, TMT, TIB and MMSE. POCD patients exhibited an initial upregulation of NRF2-related antioxidant genes, which failed to sustain at 3-months follow-up, leading to a decline in HMOX1, IP-10 and BDNF protein levels, along with increased LOX-1 protein level and NFκB expression, indicating persistent oxidative stress and inflammation. In contrast, non-POCD patients demonstrated a sustained increase in antioxidant and neuroprotective markers, suggesting a more effective compensatory response. ROC analysis identified HMOX1 and BDNF as significant predictors of POCD, with LOX-1 and IP-10 emerging as diagnostic markers at follow-up. In conclusion, our findings highlight the dynamic regulation of oxidative stress and inflammatory pathways in POCD, emphasizing the failure of sustained neuroprotection in affected patients. Further large-scale studies are necessary to validate these findings, and biomarker-based screening could facilitate early risk stratification and targeted interventions to improve cognitive outcomes after cardiac surgery.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"37"},"PeriodicalIF":3.6,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12009791/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143973322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Energy Metabolism and Brain Aging: Strategies to Delay Neuronal Degeneration.","authors":"Donghui Na, Zechen Zhang, Meng Meng, Meiyu Li, Junyan Gao, Jiming Kong, Guohui Zhang, Ying Guo","doi":"10.1007/s10571-025-01555-z","DOIUrl":"https://doi.org/10.1007/s10571-025-01555-z","url":null,"abstract":"<p><p>Aging is characterized by a gradual decline in physiological functions, with brain aging being a major risk factor for numerous neurodegenerative diseases. Given the brain's high energy demands, maintaining an adequate ATP supply is crucial for its proper function. However, with advancing age, mitochondria dysfunction and a deteriorating energy metabolism lead to reduced overall energy production and impaired mitochondrial quality control (MQC). As a result, promoting healthy aging has become a key focus in contemporary research. This review examines the relationship between energy metabolism and brain aging, highlighting the connection between MQC and energy metabolism, and proposes strategies to delay brain aging by targeting energy metabolism.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"38"},"PeriodicalIF":3.6,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12011708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting of PP2 A/GSK3β/PTEN Axis in Alzheimer Disease: The Mooting Evidence, Divine, and Devil.","authors":"Saad Misfer Alqahtani, Hayder M Al-Kuraishy, Ali I Al-Gareeb, Maha M Abdel-Fattah, Ahad Amer Alsaiari, Mubarak Alruwaili, Marios Papadakis, Athanasios Alexiou, Gaber El-Saber Batiha","doi":"10.1007/s10571-025-01554-0","DOIUrl":"https://doi.org/10.1007/s10571-025-01554-0","url":null,"abstract":"<p><p>Alzheimer disease (AD) is a progressive neurodegenerative disease of the brain due to extracellular accumulation of Aβ. In addition, intracellular accumulation of hyperphosphorlyated tau protein which form neurofibrillary tangle (NFT) is associated with progressive neuronal injury and the development of AD. Aβ and NFTs interact together to induce inflammation and oxidative stress which further induce neurodegeneration in AD. The exact relationship between Aβ and tau, the two proteins that accumulate within these lesions, has proven elusive. A growing body of work supports the notion that Aβ may directly or indirectly interact with tau to accelerate NFTs formation. Aβ can adversely affect distinct molecular and cellular pathways, thereby facilitating tau phosphorylation, aggregation, mislocalization, and accumulation. Aβ may drive tau pathology by activating specific kinases, providing a straightforward mechanism by which Aβ may enhance tau hyperphosphorylation and NFT formation. Many cellular signaling pathways such as protein phosphatase 2A (PP2A), glycogen synthase kinase 3β (GSK3β), and phosphatase and tensin homologue (PTEN) are intricate in AD neuropathology. PP2A which involved in the dephosphorylation of tau protein is deregulated in AD, and correlated with cognitive impairment. PTEN is a critical regulator of neuronal growth, survival, and development, improving synaptic plasticity and axonal regeneration. Nevertheless, mutated PTEN is associated with the development of cognitive impairment by inhibiting the expression and the activity of PP2A. Furthermore, dysregulation of GSK3β affects Aβ, tau protein phosphorylation, synaptic plasticity and other signaling pathways involved in the pathogenesis of AD. Therefore, there is a close interaction among GSK3β, PTEN, and PP2A. GSK3β exaggerates AD neuropathology by inhibiting PP2A and activates the expression of PTEN. These findings specified a related interaction among GSK3β, PTEN, and PP2A, and modulation of the single component of this axis may not produce an effective effect against AD neuropathology. Modulation of this axis by metformin and statins can reduce AD neuropathology. Therefore, this review aims to discuss the role of GSK3β/PTEN/PP2A axis in AD neuropathology and how targeting of this axis by metformin and statins can produce effective therapeutic strategy in the management of AD. In conclusion, inhibition of GSK3β and PTEN and activation of PP2A may be more suitable than modulation of single signaling pathway. Metformin and statins by activating PP2A and inhibiting of GSK3β and PTEN attenuate the development and progression of AD.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"36"},"PeriodicalIF":3.6,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12008108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143987225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research Progress in the Treatment of Postpartum Depression.","authors":"Li-Na Guan, Li Li, Hui-Hua Li, Zhen Wang, Jia-Jia Yun, Wei-Fang Ding, Gui-Ying Sun, Lin Xue","doi":"10.1007/s10571-025-01542-4","DOIUrl":"https://doi.org/10.1007/s10571-025-01542-4","url":null,"abstract":"<p><p>Postpartum depression is a common type of psychiatric disorder during the postpartum period. It significantly affects the mental and physical health of new mothers and has long-term negative effects on the growth and development of infants and toddlers. Consequently, there is increasing research both domestically and internationally on the treatment of postpartum depression, though the means of treatment are limited. This article conducted a systematic literature search in the following databases: China National Knowledge Infrastructure Journal Database, Wanfang Data Knowledge Service Platform, VIP Chinese Journal Service Platform, Pubmed Database, Web of Science, etc. This paper provides a comprehensive review of the research on pharmacological treatment, non-pharmacological treatment, and combined treatment of postpartum depression both domestically and internationally, offering a foundation for further exploration of effective clinical treatment methods for postpartum depression.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"35"},"PeriodicalIF":3.6,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12003228/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143965553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of 5 Intermediate Structural Variations of Microglia Within an Organotypic Hippocampal Slice Model After Regionalized Toxic Injury.","authors":"A Jesus Trejos, A X Francis Schanne","doi":"10.1007/s10571-025-01545-1","DOIUrl":"https://doi.org/10.1007/s10571-025-01545-1","url":null,"abstract":"<p><p>The dendritic cell of the CNS, the microglia (MG), is an initiation point of the immunological response within the post-blood-brain barrier (BBB) compartment. Microglia drastically changes in response to cell stress to a much different non-dendritic morphologies. This investigation postulates that if the first MG responses to toxic injury are isolated and studied in greater morphological detail, there is much to be learned about microglia's metamorphosis from and M2 to an M1 state. The organotypic hippocampal slice was the experimental setting used to investigate microglial response to toxic injury; this isolates dendritic cell to post-BBB cells dynamics from the impact of nonspecific of in vivo blood-derived signaling. Within the context of biochemically verified precise toxic cell injury/death (induced with mercury or cyanide in combination with 2-deoxy-glucose) to a specific region within the hippocampal slice, MG's morphological response was evaluated. There was up to 35% increase in microglia activation proximally to injury (CA3 region) and no changes distally (DG region) when compared to control slices treated with PBS. Maximum microglia activation consisted of a 3 plus-fold increase in the distance between the nucleus membrane and the cell membrane, which underscores an extensive and quantifiable amount of membrane rearrangement. This quantification can be applied to contemporaneous AI image analysis algorithms to demarcate and quantify relative MG activation in and around a site of injury. In between baseline and activated MG morphologies, 5 intermediate morphologies (or structural variations) are described as it relates to its cell body, nucleus, and dendrites. The result from this study reconciles details of MG's structure to its holistic characteristics in relation to parenchymal cell stress.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"34"},"PeriodicalIF":3.6,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11981971/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143976263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The STING Signaling: A Novel Target for Central Nervous System Diseases.","authors":"Min Song, Jianxun Ren, Zhipeng Zhu, Zhaohui Yi, Chengyun Wang, Lirong Liang, Jiahui Tian, Guofu Mao, Guohua Mao, Min Chen","doi":"10.1007/s10571-025-01550-4","DOIUrl":"10.1007/s10571-025-01550-4","url":null,"abstract":"<p><p>The canonical cyclic GMP-AMP (cGAMP) synthase (cGAS)-Stimulator of Interferon Genes (STING) pathway has been widely recognized as a crucial mediator of inflammation in many diseases, including tumors, infections, and tissue damage. STING signaling can also be activated in a cGAS- or cGAMP-independent manner, although the specific mechanisms remain unclear. In-depth studies on the structural and molecular biology of the STING pathway have led to the development of therapeutic strategies involving STING modulators and their targeted delivery. These strategies may effectively penetrate the blood-brain barrier (BBB) and target STING signaling in multiple central nervous system (CNS) diseases in humans. In this review, we outline both canonical and non-canonical pathways of STING activation and describe the general mechanisms and associations between STING activity and CNS diseases. Finally, we discuss the prospects for the targeted delivery and clinical application of STING agonists and inhibitors, highlighting the STING signaling pathway as a novel therapeutic target in CNS diseases.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"33"},"PeriodicalIF":3.6,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11977075/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulation of Hmox1 and Rpgrip1l Expression Linked to Risk-Taking Behavior, Reduced Depressive Symptoms, and Diminished Novelty Socialization in SUMO1 Knockout Mice.","authors":"Qiwei Dai, Yuxiang Wang, Hongbin Xu, He Dong, Fang Nie, Lianxue Zhang, Xiaozhi Liu, Zhiqing Li","doi":"10.1007/s10571-025-01548-y","DOIUrl":"10.1007/s10571-025-01548-y","url":null,"abstract":"<p><p>SUMO1 is involved in the normal physiological functions of the nervous system and is also associated with the development of neurodegenerative diseases. Whereas, the effects and underling mechanisms of SUMO1 knockout (SUMO1- KO) on emotion- and cognition -related behaviors remain unexplored. We investigated changes in depression-like behaviors, social interaction, and cognition in SUMO1-KO mice compared to wild-type (WT) controls using the open-field test, tail suspension test, three-chamber test and novel object recognition test, respectively. To explore the underlying mechanisms of these behavioral differences, we performed Gene Ontology (GO) analysis of proteomics data and subsequently validated the findings through experimental verification. The results showed that SUMO1-KO mice exhibited increased risk-taking behavior, reduced depressive symptoms, and diminished novelty socialization compared to WT mice. Mass spectrometry-based proteomics analysis revealed 370 upregulated proteins and downregulated 84 proteins. GO annotation analysis identified significant enrichment of amino acid transmembrane transporter activities and ion channel. We further investigated two behavior-associated proteins, Hmox1 and Rpgrip1l, and validated their downregulated expression. We concluded that decreased expression of Hmox1 and Rpgrip1l associated with the risk-taking behavior, reduced depressive symptoms, and diminished novelty socialization observed in SUMO1-KO mice.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"32"},"PeriodicalIF":3.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11961799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}