Molecular Neurobiology最新文献

{"title":"Epigenetic Mechanisms Shaping Spine Regulation: Unveiling the Role of Cytoskeletal Dynamics and Localized Protein Synthesis.","authors":"Shiwangi Gupta, Abhinoy Kishore, Vikas Rishi, Aanchal Aggarwal","doi":"10.1007/s12035-025-05045-7","DOIUrl":"10.1007/s12035-025-05045-7","url":null,"abstract":"<p><p>Spines, the anatomical specializations on nerve cells, undergo persistent remodeling that often drives synapse development and plasticity. This remodeling is primarily driven by cytoskeletal regulation and local protein synthesis, both of which shape spine morphology. The cytoskeleton, composed mainly of actin filaments and microtubules, provides structural integrity and plasticity to spines by tuning their dynamics. Complementing this, local protein synthesis supports spine growth and modification by enabling localized trafficking and translation of synaptic mRNAs. At a given time, stimuli elicit a cascade of synaptic events involving both cytoskeletal dynamics and localized translation that converge to orchestrate spine development. Importantly, these events are not governed solely by immediate cellular signaling; rather, it extends to include epigenetic modifiers that exert control over the spatial and temporal dynamics of spine development. Aberrant expression of such modifiers can disrupt spine development and contribute to synaptopathies-neurological disorders rooted from synaptic dysfunction. Previous research has cursorily examined how epigenetic regulation contributes to neurodegenerative diseases, lacking detailed exploration of epigenetics in individual synaptic events. However, understanding spine reprogramming and its epigenetic, underpinnings need to be deciphered. Emerging evidence suggests altered epigenetic profiles disturb the coordinated balance of synaptic machinery and its structural architecture. Here, we review the stochastic mechanisms influencing spine and synapse morphology, emphasizing cytoskeletal maintenance and local protein synthesis-and how these events are tuned in light of epigenetic regulation.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"15024-15054"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144208998","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":"Elevated Acetylation of MFN2 is Accompanied by the Disruption of Mitochondrial Energy Metabolism and Inflammation in a Mouse Model of Depression.","authors":"Xiaoxian Xie, Mengya Zhang, Haosheng Xu, Liangliang Wang, Lei Sun, Jiafeng Zhou, Shulin Du, Zezhi Li, Daniel C Anthony","doi":"10.1007/s12035-025-05222-8","DOIUrl":"10.1007/s12035-025-05222-8","url":null,"abstract":"<p><p>Mitofusin-2 (MFN2) is recognized as an important regulator of mitochondrial function. The activity of MFN2 is increased by deacetylation, but while MFN2 levels have been reported to be increased in major depressive disorder, the relationship between acetylation status of MFN2, mitochondrial energy production, and inflammation in depression-like disease in rodents has not been studied. Here, we induced a depression-like syndrome in mice with a 14-day-long chronic restraint stress (CRS) model, and the levels of acetylated MFN2 and SIRT1 activity were measured. The interaction of MFN2 with complex I was identified by immunoprecipitation, and the levels of mitochondrial metabolites were measured by GC-MS. MFN2 levels were unaltered by CRS, but SIRT1 expression and activity were reduced in the CRS-exposed mice, and levels of acetylated MFN2 were significantly increased. CRS affected mitochondrial energy metabolism by reducing the expression and activity of complexes I-V, decreasing levels of NAD⁺ and ATP synthase, and diminishing ATP production. Thus, while the expression of Mfn2 was unchanged by CRS, the inhibition of MFN2 deacetylation, via loss of SIRT1 activity, was associated with impaired mitochondrial oxidative phosphorylation, increased oxidative stress markers, and increased levels of inflammatory markers under the control of the SIRT1 target NFκB. The results presented here highlight the profound influence of acetylation/deacetylation-mediated control associated with depression-like behaviors.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14167-14175"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642880","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":"Prefrontal Cortex Molecular Signatures of Chronically Socially Isolated Rats and Their Response to Fluoxetine Treatment.","authors":"Dragana Filipović, Christoph W Turck","doi":"10.1007/s12035-025-05013-1","DOIUrl":"10.1007/s12035-025-05013-1","url":null,"abstract":"<p><p>Despite intensive scientific and clinical research, the pathophysiological mechanisms of major depressive disorder (MDD) are still not fully understood, impeding the discovery of new effective treatments. A significant clinical challenge is the delayed onset of antidepressant efficacy, which limits timely therapeutic intervention. Recent advances in proteomics and metabolomics offer new opportunities to explore these complexities at the molecular level. This review presents a comprehensive analysis of the biochemical alterations and affected molecular pathways associated with depressive-like behavior in adult male rats subjected to chronic social isolation stress (CSIS), a well-established rodent model of depression. Additionally, it examines the effects of fluoxetine, a selective serotonin reuptake inhibitor (SSRI) commonly used in MDD treatment, to uncover potential mechanisms underlying the drug's therapeutic action. By integrating mass spectrometry-based proteomic and metabolomic analyses of cytosolic, nonsynaptic mitochondrial, and synaptosomal-enriched fractions of the rat prefrontal cortex, an area crucially implicated in both clinical and animal models of depression, this review provides insights into state-specific molecular signatures. The findings discussed here contribute to a deeper understanding of the neurobiological basis of depression and offer novel insights into the biochemical mechanisms mediating antidepressant effects, with potential for the development of improved therapeutic strategies.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14544-14559"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144001918","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":"Linking Metabolic Syndrome to Neurodegeneration Mechanisms and Potential Treatments.","authors":"Amina Džidić-Krivić, Almir Fajkić, Esma Karahmet Farhat, Lana Lekić, Amira Ejubović, Samra Kadić Vukas, Malik Ejubović, Orhan Lepara, Emina Karahmet Sher","doi":"10.1007/s12035-025-04947-w","DOIUrl":"10.1007/s12035-025-04947-w","url":null,"abstract":"<p><p>The global rise in both metabolic syndrome (MetS) and neurodegenerative diseases (NDs), particularly dementia and Alzheimer's disease (AD) poses a growing health and socioeconomic burden. MetS affects approximately 25% of the global adult population and is associated with insulin resistance, hypertension, dyslipidemia, and obesity, factors increasingly linked to cognitive impairment and brain atrophy. This review explores the shared pathophysiological mechanisms between MetS and NDs, including neuroinflammation, oxidative stress, insulin resistance in the brain, blood-brain barrier (BBB) dysfunction, mitochondrial damage, gut microbiota dysbiosis, and alterations in the renin-angiotensin system. In terms of substance, MetS patients are four times more likely to develop dementia, with increased markers such as CRP and IL-6 present in the patient populations. The review suggests the role of astrocytic insulin signalling, adipokines, and toll-like receptors as key molecular links. Interventions such as caloric restriction, hydroxytyrosol (HT), and intranasal insulin have shown promising outcomes at preclinical and early clinical stages. Antidiabetic drugs like metformin, liraglutide, and GLP-1 receptor agonists have the potential to modulate neuroinflammation and improve cognition. Angiotensin receptor blockers like losartan and candesartan also exhibit neuroprotection via RAS pathway modulation. The review emphasizes the need for longitudinal studies and clinical trials to confirm these therapeutic agents and develop effective and cost-friendly interventions for the prevention and management of neurodegeneration in patients with metabolic syndrome.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14344-14366"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143990811","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":"Fermented Soybean Pulp Alleviates Disease Progression of 5×FAD Model Mice.","authors":"Chun-Yen Yang, Yu-Hsuan Liu, Ta-Chun Lin, Kuo-Hsuan Chang, Hsiu Mei Hsieh-Li","doi":"10.1007/s12035-025-05191-y","DOIUrl":"10.1007/s12035-025-05191-y","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is the most common neurodegenerative disorder of the central nervous system, characterized by memory loss and cognitive decline. The two main hypotheses regarding AD involve the accumulation of amyloid-β (Aβ) forming plaques and the intracellular hyperphosphorylation of tau protein, leading to the formation of neurofibrillary tangles (NFT). These processes are accompanied by neuroinflammation and oxidative stress, and eventual neuronal death. While soy foods are widely recognized for their nutritional benefits, soybean pulp (okara), the residue left over from making tofu or soybean milk, is mostly discarded as kitchen waste, despite being rich in nutrients such as dietary fiber, protein, and isoflavones. This underutilized byproduct may serve as a valuable resource for functional food development and sustainable resource use. In this study, fermented soybean pulp (FS) demonstrated neuroprotective effects. In vitro, FS at concentrations of 0.001 µg/mL and 0.01 µg/mL significantly improved cell viability in Aβ-induced HT-22 cells and reduced lipid peroxidation. Further, in vivo oral administration of FS attenuated the cognitive deficits of 5 × FAD mice, enhancing both short and long-term memory and reducing anxiety-like behaviors. Immunohistochemical analysis revealed that the FS-treated 5 × FAD mice group significantly reduced hippocampal amyloid plaque accumulation and gliosis. FS also upregulated the expression levels of brain-derived neurotrophic factor (BDNF), PSD95, and synaptophysin, while preventing hippocampal neuronal loss. Mechanistically, FS may activate the Nrf2 antioxidant pathway and NF-κB-mediated inflammation through the modulation of the Akt/GSK3β signaling axis in the hippocampus. These molecular actions likely contribute to increased antioxidant enzymes and suppressed neuroinflammatory responses. Overall, this study suggests that FS has therapeutic potential for alleviating cognitive and behavioral impairments in AD. Moreover, the repurposing of soybean pulp, which would otherwise be discarded, enhances its utilization value and supports sustainable green recycling.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14121-14139"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511221/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144637667","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":"Advances in the Research of Mesenchymal Stromal Cells in the Treatment of Maxillofacial Neurological Disorders and the Promotion of Facial Nerve Regeneration.","authors":"De-Zhi Zhao, Han-Xiao Wei, Yi-Bing Yang, Kang Yang, Fang Chen, Qian Zhang, Tao Zhang","doi":"10.1007/s12035-025-04981-8","DOIUrl":"10.1007/s12035-025-04981-8","url":null,"abstract":"<p><p>Maxillofacial neurological disorders include a range of disorders affecting the cranial nerves, which can be caused by a variety of reasons, including infection, trauma, tumor, and surgical complications, resulting in severe dysfunction, and the study of new approaches for the treatment of these disorders is crucial for the restoration of sensory and motor functions of the face. In recent years, due to the excellent tissue regenerative ability of mesenchymal stromal cells (MSCs), research on MSCs and MSC-derived exosomes has been progressively deepened, bringing many new perspectives to the therapeutic strategies for many diseases. Facial nerve regeneration is a complex process involving various pathophysiological mechanisms and therapeutic strategies to restore nerve function after injury. And the rapid development of stem cell tissue engineering has greatly facilitated the research process of facial nerve regeneration. In this paper, we review the characteristics of MSCs and neural stem cells (NSCs), the roles they play in the neural microenvironment and the mechanisms that promote nerve regeneration, summarize the research progress of MSCs in the treatment of maxillofacial neurological disorders, and highlight the promising directions for future development.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14407-14423"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971572","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":"Advancements in Stem Cell Research for Effective Therapies Against Alzheimer's Disease: Current Investigation and Future Insight.","authors":"Abhinav Gupta, Arya Ghosh, Neelima Sharma, Bapi Gorain","doi":"10.1007/s12035-025-05003-3","DOIUrl":"10.1007/s12035-025-05003-3","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is the most prevalent cause of dementia in the elderly, affecting approximately 50 million individuals globally with significant impose in health and financial burdens. Despite extensive research, no current treatment effectively halts the progression of AD, primarily due to its complex pathophysiology of the disease and the limitations of available therapeutic approaches. In this context, stem cell transplantation has emerged as a promising treatment strategy, harnessing the regenerative capabilities of various stem cell types, including neural stem cells (NSCs), embryonic stem cells (ESCs), and mesenchymal stem cells (MSCs). This review explores the potential of stem cell-based therapies in AD, emphasizing the necessity for continued innovation to overcome existing challenges and enhance therapeutic efficacy. Briefly, NSCs have shown potential in improving cognitive function and reducing AD pathology through targeted transplantation and neuroprotection; however, challenges such as optimizing transplantation protocols and ensuring effective cell integration persist. Concurrently, ESCs, with their pluripotent nature, present opportunities for modulating AD and generating therapeutic neurons, but ethical concerns and immunogenicity present significant obstacles to clinical application. Moreover, MSCs have demonstrated potential in ameliorating AD-related pathology and promoting neurogenesis, offering a more accessible alternative with fewer ethical constraints. The review concludes that the combinatory approaches of different stem cells may provide synergistic benefits in addressing AD-related pathophysiology, warranting further exploration in future research.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14560-14584"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144036632","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":"Neuron-Derived Extracellular Vesicles: Emerging Regulators in Central Nervous System Disease Progression.","authors":"Sitong Liu, Aitong Feng, Zhigang Li","doi":"10.1007/s12035-025-05010-4","DOIUrl":"10.1007/s12035-025-05010-4","url":null,"abstract":"<p><p>The diagnosis and exploration of central nervous system (CNS) diseases remain challenging due to the blood-brain barrier (BBB), complex signaling pathways, and heterogeneous clinical manifestations. Neurons, as the core functional units of the CNS, play a pivotal role in CNS disease progression. Extracellular vesicles (EVs), capable of crossing the BBB, facilitate intercellular and cell-extracellular matrix (ECM) communication, making neuron-derived extracellular vesicles (NDEVs) a focal point of research. Recent studies reveal that NDEVs, carrying various bioactive substances, can exert either pathogenic or protective effects in numerous CNS diseases. Additionally, NDEVs show significant potential as biomarkers for CNS diseases. This review summarizes the emerging roles of NDEVs in CNS diseases, including Alzheimer's disease, depression, traumatic brain injury, schizophrenia, ischemic stroke, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis. It aims to provide a novel perspective on developing therapeutic and diagnostic strategies for CNS diseases through the study of NDEVs.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14585-14612"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033710","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":"DTX1 Modulates Microglial M1 Polarization and Exacerbates Neuroinflammation in Traumatic Brain Injury Model Rats through NF-κB/IRF5.","authors":"Yonghui Zhang, Zongxing Zou, Rongwei Li, Xiaochuan Fu, Ganyu Li, Lu Wang, Yan Zhang, Yuyu Chen, Zuzhi Chen, Dongfang Yang, Yan Jiao, Weiguang Zhang, Tieniu Mei, Liang Tan, Ying Cao, Changlin Yin","doi":"10.1007/s12035-025-05200-0","DOIUrl":"10.1007/s12035-025-05200-0","url":null,"abstract":"<p><p>Microglial polarization is crucial in the pathogenesis of traumatic brain injury (TBI), yet the underlying regulatory mechanisms remain incompletely understood. In this study, we investigated the role of Deltex E3 ubiquitin ligase 1 (DTX1) in modulating microglial polarization and neuroinflammation following TBI. We established a rat TBI model and conducted both gain- and loss-of-function experiments by delivering adenoviral vectors encoding DTX1 or siRNA-DTX1-liposome complexes in vivo (into the injured rat brain) and in vitro (into cultured microglial cells). We found that that DTX1 expression was significantly upregulated in lipopolysaccharide (LPS)-stimulated microglia and in post-TBI rat brains. Overexpression of DTX1 promoted proinflammatory cytokine production and shifted microglia toward the M1 phenotype, as indicated by elevated inducible nitric oxide synthase (iNOS) and reduced arginase-1 (Arg1). Conversely, silencing DTX1 decreased iNOS and increased Arg1 expression, indicative of a shift toward the anti-inflammatory M2 phenotype. In vivo, DTX1 overexpression exacerbated neuroinflammation and cognitive deficits, whereas DTX1 knockdown mitigated these outcomes. In summary, these results identify DTX1 as a critical regulator of microglial polarization and neuroinflammation and suggest its potential as a therapeutic target for TBI.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14140-14155"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511207/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144637664","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":"EP300 Regulates CD8br AC (TBNK Panel) to Facilitate Insomnia.","authors":"Xin Men, Qian Wang","doi":"10.1007/s12035-025-05188-7","DOIUrl":"10.1007/s12035-025-05188-7","url":null,"abstract":"<p><p>Insomnia is a prevalent clinical condition that is caused by the interaction of environmental, inflammatory, immune system, physiological, and psychological factors. Nevertheless, the significance of lactylation-related gene in the pathogenesis of insomnia remains unknown. The causal relationship between lactylation-related gene and insomnia was initially analyzed using Mendelian randomization. Exposure was determined using cis-expression quantitative trait loci (cis-eQTL) from the Expression Quantitative Trait Locus Gen (eQTLGen) consortium. We obtained insomnia from the FinnGen database, which comprises 490,763 controls and 6776 cases. Subsequently, we performed a difference analysis of the Gene Expression Omnibus (Geo) data on insomnia and a summary-data-based MR (SMR) analysis to further validate our findings. We used a mediation approach by immune cells to study the effect of lactylation-related genes on insomnia. We identified one lactylation-related gene associated with insomnia. EP300 also passed the SMR test (p < 0.05), and heterogeneity was assessed using the auxiliary heterogeneity in dependent instruments (HEIDI) test (p > 0.05). Using data from the Geo database, the overall difference in EP300 expression between insomnia patients and healthy individuals was compared and found to be significant. A mediation analysis was employed to investigate the impact of immune cells and EP300 on insomnia. We found that EP300 may promote insomnia by regulating the CD8br AC (TBNK panel). This provides new insights into the relationship between lactylation-related genes and insomnia and serves as a novel therapeutic target for future research.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"13989-13998"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511179/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144591759","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}