Frontiers in Cellular Neuroscience最新文献

{"title":"Sialylation as a checkpoint for inflammatory and complement-related retinal diseases.","authors":"Yiduo Min, German Cuevas-Rios, Thomas Langmann, Harald Neumann","doi":"10.3389/fncel.2025.1623755","DOIUrl":"10.3389/fncel.2025.1623755","url":null,"abstract":"<p><p>Sialylation is a modification process involving the addition of sialic acid residues to the termini of glycoproteins and glycolipids in mammalian cells. Sialylation serves as a crucial checkpoint inhibitor of the complement and immune systems, particularly within the central nervous system (CNS), including the retina. Complement factor H (FH), complement factor properdin (FP), and sialic acid-binding immunoglobulin-like lectin (SIGLEC) receptors of retinal mononuclear phagocytes are key players in regulating the complement and innate immune systems in the retina by recognizing sialic acid (Sia) residues. Intact retinal sialylation prevents any long-lasting and excessive complement or immune activation in the retina. However, sialylated glycolipids are reduced in the CNS with aging, potentially contributing to chronic inflammatory processes in the retina. Particularly, genetically induced hyposialylation in mice leads to age-related, complement factor C3-mediated retinal inflammation and bipolar cell loss. Notably, most of the gene transcript pathways enriched in the mouse retina, following genetically induced hyposialylation, are also involved in age-related macular degeneration (AMD). Interestingly, intravitreal application of polysialic acid (polySia) controlled the innate immune responses in the mouse retina by blocking mononuclear phagocyte reactivity, inhibiting complement activation, and protecting against vascular damage in two different humanized SIGLEC-11 animal models. Accordingly, a polySia polymer conjugate has entered clinical phase II/III testing in patients with geographic atrophy secondary to AMD. Thus, hyposialylation or dysfunctional sialylation should be considered as an age-related contributor to inflammatory retinal diseases, such as AMD. Consequently, sialic acid-based biologics could provide novel therapies for complement-related retinal diseases.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1623755"},"PeriodicalIF":4.2,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12245909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625750","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":"PTEN in somatostatin neurons regulates fear and anxiety and is required for inhibitory synaptic connectivity within central amygdala.","authors":"Timothy W Holford, Kaitlyn N Letourneau, Carolyn Von-Walter, Daniela Moncaleano, Cody L Loomis, M McLean Bolton","doi":"10.3389/fncel.2025.1597131","DOIUrl":"10.3389/fncel.2025.1597131","url":null,"abstract":"<p><strong>Introduction: </strong>The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a negative regulator of the mTOR pathway and is strongly associated with autism spectrum disorder (ASD), with up to 25% of ASD patients with macrocephaly harboring PTEN mutations. Mice with germline PTEN haploinsufficiency show behavioral characteristics resembling ASD, as do various mouse models with conditional knockouts of PTEN. Human tissue studies and those from multiple genetic mouse models suggest that dysfunction of GABAergic interneurons may play a role in the development of ASD, but the precise mechanisms remain elusive. PTEN provides a target for investigation because it regulates the development of inhibitory neurons arising from the medial ganglionic eminence, promoting the survival and maturation of parvalbumin (PV+) neurons at the expense of somatostatin (SOM+) neurons.</p><p><strong>Methods: </strong>Here, we investigate how PTEN regulates SOM+ neurons at the cellular and circuit level in the central lateral amygdala (CeL), an area that governs the key ASD behavioral symptoms of social anxiety and altered emotional motivation for social engagement using behavioral analysis, electrophysiology, and two-photon local circuit mapping.</p><p><strong>Results: </strong>We found that knocking out PTEN in SOM+ neurons results in elevated levels of fear and anxiety and decreases CeL local circuit connectivity. Specifically, this manipulation decreased the strength of connections between individual neurons and altered the distribution of local connections in a cell-type specific manner. In contrast to the deficit in local inhibitory connections within CeL, the excitatory drive from the major CeL input, the basolateral amygdala (BLA) was enhanced.</p><p><strong>Discussion: </strong>This combined imbalance of enhanced excitation and diminished local inhibition likely underlies the heightened fear learning and anxiety we observed in the PTEN-SOM-KO mice.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1597131"},"PeriodicalIF":4.2,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12240933/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607921","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":"Is environmental enrichment effective in modulating autophagy markers in the brain exposed to adverse conditions? A systematic review.","authors":"Clarice Beatriz Gonçalves Silva, Matheus Santos de Sousa Fernandes, Debora Dantas Nucci Cerqueira, Gabriela Carvalho Jurema Santos, Fatma Hilal Yagin, Yalin Aygun, Georgian Badicu, Fabiana S Evangelista, Pablo Prieto-González, Fabrício Oliveira Souto, Ashit Kumar Dutta, Sameer Badri Al-Mhanna, Abedelmalek Kalefh Tabnjh","doi":"10.3389/fncel.2025.1624500","DOIUrl":"10.3389/fncel.2025.1624500","url":null,"abstract":"<p><p>Autophagy is a key regulator of cellular homeostasis and neuronal survival, particularly under adverse physiological conditions. Environmental enrichment (EE), a non-pharmacological intervention providing enhanced sensory, cognitive, and motor stimulation, may modulate autophagic processes in the brain. This systematic review aimed to synthesize preclinical findings on the effects of EE on autophagy markers in rodent models subjected to diverse adverse conditions. A literature search across PubMed, Scopus, ScienceDirect, and embase yielded eight eligible studies meeting inclusion criteria. EE was found to be generally associated with upregulation of key autophagic markers such as Beclin-1, LC3-II/LC3-I ratio, cathepsins, p62, p-TFEB, and LAMP-1 across brain regions including the cortex, hippocampus, and penumbral area. However, reductions in some markers were also observed, indicating that the modulatory effects of EE are context-dependent and may vary with disease model, brain region, or EE protocol duration. These findings suggest that EE holds promise as an adjunctive strategy to modulate autophagy and mitigate neurodegeneration, though heterogeneity in study design and outcomes warrants caution during interpretation. Further mechanistic and sex-specific studies are needed to clarify the therapeutic relevance of EE-induced autophagic modulation.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1624500"},"PeriodicalIF":4.2,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12238764/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599915","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":"The role of oxidative stress in spinal cord ischemia reperfusion injury: mechanisms and therapeutic implications.","authors":"Yu Xing, Yuan-Zhang Xiao, Min Zhao, Jiang-Jun Zhou, Kai Zhao, Chun-Lin Xiao","doi":"10.3389/fncel.2025.1590493","DOIUrl":"10.3389/fncel.2025.1590493","url":null,"abstract":"<p><p>Spinal cord ischemia/reperfusion injury (SCIRI) is a serious disease that leads to the loss of sensory and motor functions and is a common complication after spinal cord injury, spinal cord degeneration or thoracic and abdominal aortic surgery. At present, the spinal cord is mainly protected from ischemic injury through treatment strategies such as hypothermia, surgery and drug assistance, but these intervention measures cannot effectively improve these conditions. SCIRI is a complex process that leads to cell damage and death. Among them, oxidative stress is an important pathological event of ischemia/reperfusion injury. Oxidative stress can initiate multiple inflammatory and apoptotic pathways, triggering a series of destructive events such as inflammatory responses and cell death, further deteriorating the microenvironment at the injured site, and leading to neurological dysfunction. Based on the important role of oxidative stress in SCIRI, we believe that targeted inhibition of oxidative stress responses can effectively reduce secondary injuries caused by trauma, which has a certain positive effect on the rehabilitation and prognosis of patients with SCIRI. This review systematically expounds the spatiotemporal dynamic characteristics of oxidative stress during the SCIRI process and its molecular regulatory network, with a focus on analyzing the multivariate generation mechanism of ROS. To deeply explore the regulatory effects of ROS on pathological processes such as neuronal death, inflammatory response and blood-spinal barrier disruption under SCIRI conditions, as well as its interaction patterns with signaling pathways. In order to form a systematic treatment for SCIRI caused by oxidative stress and promote the recovery of neurological function after injury. This review is helpful for us to understand the effect of oxidative stress on SCIRI and provides a theoretical basis for the treatment of SCIRI based on oxidative stress.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1590493"},"PeriodicalIF":4.2,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590843","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":"Corrigendum: <i>O</i> ⁶-methylguanine DNA methyltransferase (MGMT) expression in U1242 glioblastoma cells enhances <i>in vitro</i> clonogenicity, tumor implantation <i>in vivo</i>, and <i>sensitivity</i> to alisertib-carboplatin combination treatment.","authors":"Müge Sak, Brian J Williams, Andrew J Hey, Mayur Sharma, Leslie Schier, Megan J Wilson, Mahatma Ortega, Alyssa I Lara, Mikaela N Brentlinger, Norman L Lehman","doi":"10.3389/fncel.2025.1637837","DOIUrl":"10.3389/fncel.2025.1637837","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fncel.2025.1552015.].</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1637837"},"PeriodicalIF":4.2,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590842","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":"Knockdown and overexpression of basolateral amygdala SIRT1 via AAV bidirectionally alter morphine-induced conditioned place preference extinction in mice.","authors":"Guo Hao, Yao Mingchen, Zheng Yalin, Qu Yaqi, Yang Tingwu, Xing Xinru, Li Kaixuan, Dong Yani, Liu Dongsen","doi":"10.3389/fncel.2025.1604914","DOIUrl":"10.3389/fncel.2025.1604914","url":null,"abstract":"<p><strong>Introduction: </strong>This study investigates the role of SIRT1 in basolateral amygdala (BLA) glutamatergic neurons in morphine-induced conditioned place preference (CPP).</p><p><strong>Methods: </strong>Via SIRT1 knockdown/overexpression in bilateral BLA of morphine-induced CPP mice. Outcomes measured by behavioral tests, WB, and transmission electron microscopy.</p><p><strong>Results: </strong>We found that SIRT1 knockdown prolonged CPP extinction and enhanced reinstatement, whereas overexpression accelerated extinction and attenuated relapse. Behavioral tests revealed that SIRT1 knockdown rescued morphine-induced memory impairment and anxiety-like behaviors, while overexpression exacerbated these effects. Ultrastructural and molecular analyses demonstrated SIRT1 modulation of synaptic plasticity-related proteins (BDNF, PSD95) and synaptic ultrastructure in BLA.</p><p><strong>Discussion: </strong>Our findings reveal that SIRT1 bidirectionally regulates opioid-associated memory persistence through synaptic remodeling, highlighting its potential as an epigenetic target for addiction treatment. While SIRT1 is implicated in neuroplasticity, its specific role in modulating opioid-associated memory circuits within the BLA remains undefined, representing a critical gap in understanding addiction neuropathology.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1604914"},"PeriodicalIF":4.2,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575206","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":"Establishment of an AI-supported scoring system for neuroglial cells.","authors":"Annika Bitsch, Manfred Henrich, Svenja Susanne Erika Körber, Kathrin Büttner, Christiane Herden","doi":"10.3389/fncel.2025.1584422","DOIUrl":"10.3389/fncel.2025.1584422","url":null,"abstract":"<p><p>The feasibility of a computer-aided scoring system based on artificial intelligence to detect and classify morphological changes in neuroglial cells was assessed in this study. The system was applied to hippocampal organotypic slice cultures (OHC) from 5 to 7 day-old wild-type and TNF-overexpressing mice in order to analyze effects of a proinflammtory stimulus such as TNF. The area fraction of cells, cell number, number of cell processes and area of the cell nucleus were used as target variables. Immunfluorescence labeling was used to visualize neuronal processes (anti-neurofilaments), microglia (anti-Iba1) and astrocytes (anti-GFAP). The analytic system was able to reliably detect differences in the applied target variables such as the increase in neuronal processes over a period of 14 days in both mouse lines. The number of microglial projections and the microglial cell number provided reliable information about activation level. In addition, the area of microglial cell nuclei was suitable for classification of microglia into activity levels. This scoring system was supported by description of morphology, using the automatically created cell masks. Therefore, this scoring system is suitable for morphological description and linking the morphology with the respective cellular activity level employing analyses of large data sets in a short time.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1584422"},"PeriodicalIF":4.2,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12222295/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559667","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":"Evaluation of retinal structure changes with AI-based OCT image segmentation for sodium iodate induced retinal degeneration.","authors":"Yong Zeng, Jiaming Zhou, Yichao Li, Bruno Alvisio, Jacob Czech, David Bissig, Haohua Qian","doi":"10.3389/fncel.2025.1605639","DOIUrl":"10.3389/fncel.2025.1605639","url":null,"abstract":"<p><p>Segmentations of retinal optical coherence tomography (OCT) images provide valuable information about each specific retinal layer. However, processing images from degenerative retina remains challenging. This study developed artificial intelligence (AI)-based segmentation to analyze structure changes in sodium iodate (SI)-treated mice. The software is capable of segmenting seven retinal layers and one choroid layer. Analyzing OCT images captured at days post SI-injection (PI) revealed early changes in the retinal pigment epithelium (RPE) layer, with increase in thickness and reduction in reflectance calculated by estimated Attenuation Coefficients (eAC). On the other hand, eAC for outer nuclear layer (ONL) exhibited early and sustained increase after SI treatment. SI induced exponential reduction in ONL thickness with a half-reduction time of about 3 days, indicating progressive photoreceptor degeneration. The extent of degeneration was correlated with ONL eAC level at PI1. Inner retinal layers showed bi-phasic reactions, with initial increases in layer thickness that peaked at around PI3, followed by gradual reduction to lower than baseline levels. In addition, SI also induced transient increases in vitreous particles concentrated around the optic nerve head. Furthermore, there was a gradual reduction of choroid thickness after SI treatment. These results indicate the AI-segmentation tool's usefulness for providing a sensitive and accurate assessment of structure changes in diseased retina and revealed more detailed characterization of SI-induced degeneration in all retinal layers with distinct time courses. Our results also support ONL reflectance changes as an early biomarker for retinal degeneration.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1605639"},"PeriodicalIF":4.2,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12213626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552825","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":"Average miniature post-synaptic potential size is inversely proportional to membrane capacitance across neocortical pyramidal neurons of different sizes.","authors":"Martynas Dervinis, Guy Major","doi":"10.3389/fncel.2025.1590157","DOIUrl":"10.3389/fncel.2025.1590157","url":null,"abstract":"<p><p>In chemical synapses of the central nervous system (CNS), information is transmitted via the presynaptic release of a vesicle (or 'quantum') of neurotransmitter, which elicits a postsynaptic electrical response with an amplitude termed the 'quantal size.' Measuring amplitudes of miniature postsynaptic currents (mPSCs) or potentials (mPSPs) at the cell soma is generally thought to offer a technically straightforward way to estimate quantal sizes, as each of these miniature responses (or minis) is generally thought to be elicited by the spontaneous release of a single neurotransmitter vesicle. However, in large highly-branched neurons, a somatically recorded mini is typically massively attenuated compared with at its input site, and a significant fraction are indistinguishable from (or canceled out by) background noise fluctuations. Here, using a new software package called 'minis,' we describe a novel quantal analysis method that estimates the effective 'electrical sizes' of synapses by comparing events detected in somatic recordings from the same neuron of (a) <i>real</i> minis and (b) background noise (with minis blocked pharmacologically) with <i>simulated</i> minis added by a genetic algorithm. The estimated minis' distributions reveal a striking inverse dependence of mean excitatory mPSP amplitude on total cell membrane capacitance (proportional to cell size, or more exactly, extracellular membrane surface area) suggesting that, in rat somatosensory cortex at least, the average charge injected by single excitatory synapses (ca. 30 fC) is conserved across neocortical pyramidal neurons of very different sizes (across a more than three-fold range).</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1590157"},"PeriodicalIF":4.2,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12213790/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552805","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":"Research progress on the mechanisms of endogenous neural stem cell differentiation in spinal cord injury repair.","authors":"Tianwei Wang, Qing Han, Shi Lv, Li-Ping Zhang, Hengrui Li, Jian Liu, Jinyi Kuang, Bao-Liang Sun, Jing-Yi Sun","doi":"10.3389/fncel.2025.1592297","DOIUrl":"10.3389/fncel.2025.1592297","url":null,"abstract":"<p><p>Spinal cord injury (SCI) is a devastating condition with limited self-repair capacity, resulting in long-term disabilities. Endogenous neural stem cells (eNSCs), which are present in the adult central nervous system (CNS), hold significant potential for repairing neural damage following SCI. These cells can proliferate, migrate to the injury site, and differentiate into various neural cell types, including neurons and glial cells. However, after SCI, eNSCs predominantly differentiate into astrocytes, with minimal neuronal differentiation, thereby hindering effective neural regeneration. This review summarizes the key mechanisms underlying the differentiation of eNSCs into neurons, focusing on the molecular signaling pathways that regulate their fate, including the Notch, Wnt/β-catenin, Sonic Hedgehog, and PI3K/Akt pathways. It also discusses the microenvironment's role, including factors such as hypoxia, extracellular matrix components, and inflammatory cytokines, which influence eNSCs differentiation. The review also highlights potential therapeutic strategies to enhance eNSCs differentiation into neurons, including biomaterials and multimodal approaches that combine pharmacological, physical, and tissue engineering techniques. Despite progress in understanding eNSCs biology and signaling mechanisms, challenges remain in optimizing therapeutic strategies for SCI repair. Future research should focus on overcoming these limitations, emphasizing refining treatment timing, drug delivery systems, and the development of personalized therapies to promote effective neural regeneration and functional recovery after SCI.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1592297"},"PeriodicalIF":4.2,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12213763/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552826","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}