Journal of Neuroinflammation最新文献

{"title":"Correction: Progesterone attenuates Th17-cell pathogenicity in autoimmune uveitis via Id2/Pim1 axis.","authors":"Xiuxing Liu, Chenyang Gu, Jianjie Lv, Qi Jiang, Wen Ding, Zhaohao Huang, Yidan Liu, Yuhan Su, Chun Zhang, Zhuping Xu, Xianggui Wang, Wenru Su","doi":"10.1186/s12974-025-03412-8","DOIUrl":"https://doi.org/10.1186/s12974-025-03412-8","url":null,"abstract":"","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"99"},"PeriodicalIF":9.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microglia determine an immune-challenged environment and facilitate ibuprofen action in human retinal organoids.","authors":"Verena Schmied, Medina Korkut-Demirbaş, Alessandro Venturino, Juan Pablo Maya-Arteaga, Sandra Siegert","doi":"10.1186/s12974-025-03366-x","DOIUrl":"https://doi.org/10.1186/s12974-025-03366-x","url":null,"abstract":"<p><p>Prenatal immune challenges pose significant risks to human embryonic brain and eye development. However, our knowledge about the safe usage of anti-inflammatory drugs during pregnancy is still limited. While human induced pluripotent stem cells (hIPSC)-derived brain organoid models have started to explore functional consequences upon viral stimulation, these models commonly lack microglia, which are susceptible to and promote inflammation. Furthermore, microglia are actively involved in neuronal development. Here, we generate hIPSC-derived microglia precursor cells and assemble them into retinal organoids. Once the outer plexiform layer forms, these hIPSC-derived microglia (iMG) fully integrate into the retinal organoids. Since the ganglion cell survival declines by this time in 3D-retinal organoids, we adapted the model into 2D and identify that the improved ganglion cell number significantly decreases only with iMG presence. In parallel, we applied the immunostimulant POLY(I:C) to mimic a fetal viral infection. While POLY(I:C) exposure alters the iMG phenotype, it does not hinder their interaction with ganglion cells. Furthermore, iMG significantly enhance the supernatant's inflammatory secretome and increase retinal cell proliferation. Simultaneous exposure with the non-steroidal anti-inflammatory drug (NSAID) ibuprofen dampens POLY(I:C)-mediated changes of the iMG phenotype and ameliorates cell proliferation. Remarkably, while POLY(I:C) disrupts neuronal calcium dynamics independent of iMG, ibuprofen rescues this effect only if iMG are present. Mechanistically, ibuprofen targets the enzymes cyclooxygenase 1 and 2 (COX1/PTGS1 and COX2/PTGS2) simultaneously, from which iMG mainly express COX1. Selective COX1 blockage fails to restore the calcium peak amplitude upon POLY(I:C) stimulation, suggesting ibuprofen's beneficial effect depends on the presence and interplay of COX1 and COX2. These findings underscore the importance of microglia in the context of prenatal immune challenges and provide insight into the mechanisms by which ibuprofen exerts its protective effects during embryonic development.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"98"},"PeriodicalIF":9.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of EED-mediated histone methylation alleviates neuroinflammation by suppressing WNT-mediated dendritic cell migration.","authors":"Wenxiang Hong, Hongbo Ma, Zhibin Li, Yiwen Du, Wenjing Xia, Han Yin, Han Huang, Zebing Sun, Renhua Gai, Lexian Tong, Hong Zhu, Jincheng Wang, Bo Yang, Qiaojun He, Qinjie Weng, Jiajia Wang","doi":"10.1186/s12974-025-03429-z","DOIUrl":"10.1186/s12974-025-03429-z","url":null,"abstract":"<p><p>The epigenetic modification of histone H3 lysine 27 trimethylation (H3K27me3) by the embryonic ectoderm development (EED) protein is closely associated with the regulation of transcriptional programs and is implicated in autoimmune diseases. However, the efficacy of targeting H3K27me3 for the treatment of neuroinflammation remains unclear. In this study, we demonstrate that systemic administration of an EED inhibitor diminishes the inflammatory response mediated by dendritic cells (DCs), thereby alleviating experimental autoimmune encephalitis (EAE), a representative mouse model of autoimmune diseases in the central nervous system (CNS). Our findings indicate that EED inhibitors suppress DC migration by upregulating genes in the WNT signaling pathway that are epigenetically marked by H3K27me3. Conversely, inhibiting the WNT pathway partially reverses the impaired DC migration caused by EED inhibitors. Additionally, the genetic deletion of Eed inhibits DC migration and effectively mitigates autoimmune symptoms and inflammatory infiltration into the CNS in EAE. These results highlight EED as a critical regulator of DC migration and suggest its potential as a therapeutic target for autoimmune disorders.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"97"},"PeriodicalIF":9.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11963263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143764191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microglia efferocytosis: an emerging mechanism for the resolution of neuroinflammation in Alzheimer's disease.","authors":"Yongping Chen, Yuhong Kou, Yang Ni, Haotian Yang, Cailin Xu, Honggang Fan, Huanqi Liu","doi":"10.1186/s12974-025-03428-0","DOIUrl":"10.1186/s12974-025-03428-0","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by significant neuroinflammatory responses. Microglia, the immune cells of the central nervous system, play a crucial role in the pathophysiology of AD. Recent studies have indicated that microglial efferocytosis is an important mechanism for clearing apoptotic cells and cellular debris, facilitating the resolution of neuroinflammation. This review summarizes the biological characteristics of microglia and the mechanisms underlying microglial efferocytosis, including the factors and signaling pathways that regulate efferocytosis, the interactions between microglia and other cells that influence this process, and the role of neuroinflammation in AD. Furthermore, we explore the role of microglial efferocytosis in AD from three perspectives: its impact on the clearance of amyloid plaques, its regulation of neuroinflammation, and its effects on neuroprotection. Finally, we summarize the current research status on enhancing microglial efferocytosis to alleviate neuroinflammation and improve AD, as well as the future challenges of this approach as a therapeutic strategy for AD.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"96"},"PeriodicalIF":9.3,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11955113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuron-restricted cytomegalovirus latency in the central nervous system regulated by CD4⁺ T-cells and IFN-γ.","authors":"Fran Krstanović, Andrea Mihalić, Ahmad Seyar Rashidi, Katarzyna M Sitnik, Zsolt Ruzsics, Luka Čičin-Šain, Georges M G M Verjans, Stipan Jonjić, Ilija Brizić","doi":"10.1186/s12974-025-03422-6","DOIUrl":"10.1186/s12974-025-03422-6","url":null,"abstract":"<p><p>All human herpesviruses establish latency following the resolution of the primary infection. Among these, α-herpesviruses HSV-1, HSV-2 and VZV establish latency in neurons, whereas neurons are not traditionally considered a site of latency for other herpesviruses. Using a combination of in vivo murine models and ex vivo human fetal tissues, we discovered that cytomegalovirus (CMV), a ubiquitous β-herpesvirus, can persist in neurons and that CD4⁺ T-cell-derived interferon-gamma is critical in restricting active viral replication in this cell type. Furthermore, we show that mouse CMV can establish latency in neurons and that CD4⁺ T-cells are essential in preventing viral reactivation. Our findings may have translational significance because human cytomegalovirus (HCMV) is the leading cause of congenital viral infections resulting in neurodevelopmental and neuroinflammatory lesions with long-term functional sequelae.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"95"},"PeriodicalIF":9.3,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954325/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143743023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Akkermansia mono-colonization modulates microglia and astrocytes in a strain specific manner.","authors":"Luke A Schwerdtfeger, Toby B Lanser, Federico Montini, Thais Moreira, Danielle S LeServe, Laura M Cox, Howard L Weiner","doi":"10.1186/s12974-025-03417-3","DOIUrl":"10.1186/s12974-025-03417-3","url":null,"abstract":"<p><p>Microglia and astrocytes are the primary glial cells in the central nervous system (CNS) and their function is shaped by multiple factors. Regulation of CNS glia by the microbiota have been reported, although the role of specific bacteria has not been identified. We colonized germ-free mice with the type strain Akkermansia muciniphila (Am^T) and a novel A. muciniphila strain BWH-H3 (Am-H3) isolated from a subject with multiple sclerosis and compared to mice colonized with Bacteroides cellulosilyticus strain BWH-E5 (Bc) isolated from a healthy control subject. We then investigated the effect of these bacteria on microglia and astrocyte gene expression by RNA sequencing. We found altered gene expression profiles in brain microglia, with Akkermansia downregulating genes related to antigen presentation and cell migration. Furthermore, we observed strain specific effects, with Akkermansia H3 upregulating histone and protein binding associated genes and downregulating channel and ion transport genes. Astrocyte pathways that were altered by Akkermansia H3 mono-colonization included upregulation of proliferation pathways and downregulation in cytoskeletal associated genes. Furthermore, animals colonized with type strain Akkermansia and strain H3 had effects on the immune system including elevated splenic γδ-T cells and increased IFNγ production in CD4 + T cells. We also measured intestinal short chain fatty acids and found that both A. muciniphila strains produced proprionate while B. cellulosilyticus produced acetate, proprionate, and isovalerate. Taken together, our study shows that specific members of the intestinal microbiota influence both microglial and astroyctes which may be mediated by changes in short chain fatty acids and peripheral immune signaling.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"94"},"PeriodicalIF":9.3,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11951737/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dopamine-driven increase in IL-1β in myeloid cells is mediated by differential dopamine receptor expression and exacerbated by HIV.","authors":"Stephanie M Matt, Rachel Nolan, Samyuktha Manikandan, Yash Agarwal, Breana Channer, Oluwatofunmi Oteju, Marzieh Daniali, Joanna A Canagarajah, Teresa LuPone, Krisna Mompho, Kaitlyn Runner, Emily Nickoloff-Bybel, Benjamin Li, Meng Niu, Johannes C M Schlachetzki, Howard S Fox, Peter J Gaskill","doi":"10.1186/s12974-025-03403-9","DOIUrl":"10.1186/s12974-025-03403-9","url":null,"abstract":"<p><p>The catecholamine neurotransmitter dopamine is classically known for regulation of central nervous system (CNS) functions such as reward, movement, and cognition. Increasing evidence also indicates that dopamine regulates critical functions in peripheral organs and is an important immunoregulatory factor. We have previously shown that dopamine increases NF-κB activity, inflammasome activation, and the production of inflammatory cytokines such as IL-1β in human macrophages. As myeloid lineage cells are central to the initiation and resolution of acute inflammatory responses, dopamine-mediated dysregulation of these functions could both impair the innate immune response and exacerbate chronic inflammation. However, the exact pathways by which dopamine drives myeloid inflammation are not well defined, and studies in both rodent and human systems indicate that dopamine can impact the production of inflammatory mediators through both D1-like dopamine receptors (DRD1, DRD5) and D2-like dopamine receptors (DRD2, DRD3, and DRD4). Therefore, we hypothesized that dopamine-mediated production of IL-1β in myeloid cells is regulated by the ratio of different dopamine receptors that are activated. Our data in primary human monocyte-derived macrophages (hMDM) indicate that DRD1 expression is necessary for dopamine-mediated increases in IL-1β, and that changes in the expression of DRD2 and other dopamine receptors can alter the magnitude of the dopamine-mediated increase in IL-1β. Mature hMDM have a high D1-like to D2-like receptor ratio, which is different relative to monocytes and peripheral blood mononuclear cells (PBMCs). We further confirm in human microglia cell lines that a high ratio of D1-like to D2-like receptors promotes dopamine-induced increases in IL-1β gene and protein expression using pharmacological inhibition or overexpression of dopamine receptors. RNA-sequencing of dopamine-treated microglia shows that genes encoding functions in IL-1β signaling pathways, microglia activation, and neurotransmission increased with dopamine treatment. Finally, using HIV as an example of a chronic inflammatory disease that is substantively worsened by comorbid substance use disorders (SUDs) that impact dopaminergic signaling, we show increased effects of dopamine on inflammasome activation and IL-1β in the presence of HIV in both human macrophages and microglia. These data suggest that use of addictive substances and dopamine-modulating therapeutics could dysregulate the innate inflammatory response and exacerbate chronic neuroimmunological conditions like HIV. Thus, a detailed understanding of dopamine-mediated changes in inflammation, in particular pathways regulating IL-1β, will be critical to effectively tailor medication regimens.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"91"},"PeriodicalIF":9.3,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11931822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early control of cochlear viral load limits cochlear inflammation and prevents virus-induced sensorineural hearing loss.","authors":"Matthew D Smith, Maria C Seleme, Tatiana Marquez-Lago, Jiung-Wen Chen, Michael Mach, William J Britt","doi":"10.1186/s12974-025-03416-4","DOIUrl":"10.1186/s12974-025-03416-4","url":null,"abstract":"<p><p>Human cytomegalovirus (HCMV) is the most common viral infection acquired in utero and a leading cause of neurodevelopmental abnormalities, including sensorineural hearing loss (SNHL). In previous studies using a murine model of HCMV induced SNHL, hearing loss was correlated with virus-induced cochlear inflammation but not cochlear viral load. However, these previous findings were determined at the time of auditory testing, a time poiont well past critical periods of auditory development. In the current study, cochlear virus load early in auditory development could be correlated with the magnitude of virus-induced cochlear inflammation, cochlear histopathology and the development of hearing loss. Transcriptional profiling at early times after infection revealed dysregulation of multiple well described deafness-related genes (DRG). Treatment with antiviral antibodies early after infection decreased cochlear virus load, cochlear inflammation, cochlear histopathology, and normalized DRG expression arguing that virus-induced cochlear inflammation can result in pleiotropic effects on the developing auditory system. Finally, this model also demonstrated that sterilizing immunity was unnecessary for prevention of SNHL, thus providing a rationale for inteventions that could limit, but not completely prevent HCMV infection of the developing auditory system.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"92"},"PeriodicalIF":9.3,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11931849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhancing TREM2 expression activates microglia and modestly mitigates tau pathology and neurodegeneration.","authors":"Kai Chen, Fuyao Li, Shuwen Zhang, Yixing Chen, Tadafumi C Ikezu, Zonghua Li, Yuka A Martens, Wenhui Qiao, Axel Meneses, Yiyang Zhu, Gisela Xhafkollari, Guojun Bu, Na Zhao","doi":"10.1186/s12974-025-03420-8","DOIUrl":"10.1186/s12974-025-03420-8","url":null,"abstract":"<p><p>TREM2, a microglia-specific receptor, is strongly associated with Alzheimer's disease (AD) risk, mediating microglial responses to amyloid pathology critical to AD development. However, its role in tau pathology and neurodegeneration remains unclear. Using the PS19 tauopathy mouse model with inducible overexpression of human wild-type TREM2 (TREM2-WT) or the R47H variant (TREM2-R47H), we show that increasing TREM2-WT expression modestly reduces soluble phosphorylated tau levels and mildly preserves neuronal integrity. Single-cell RNA sequencing reveals that TREM2-WT robustly enhances microglial activation, characterized by a disease-associated microglia (DAM) signature. In contrast, TREM2-R47H overexpression exhibits a loss-of-function phenotype, with no significant impact on tau levels, neurodegeneration, or microglial activation. These findings highlight the role of TREM2 in modulating microglial activity and its influence on tau pathology and neurodegeneration, providing important insights for the future development of therapies targeting TREM2 or microglial pathways in AD or other tauopathies.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"93"},"PeriodicalIF":9.3,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11931752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MAIT cell deficiency exacerbates neuroinflammation in P301S human tau transgenic mice.","authors":"Yuanyue Zhang, Zhi Yang, Na Jiang, Xiaosheng Tan, Peng Jiang, Gaoyuan Cao, Qi Yang","doi":"10.1186/s12974-025-03413-7","DOIUrl":"10.1186/s12974-025-03413-7","url":null,"abstract":"<p><strong>Background: </strong>The role of immune cells in neurodegeneration remains incompletely understood. Accumulation of misfolded tau proteins is a hallmark of neurodegenerative diseases. Our recent study revealed the presence of mucosal-associated invariant T (MAIT) cells in the meninges, where they express antioxidant molecules to maintain meningeal barrier integrity. However, the role of MAIT cells in tau-related neuroinflammation and neurodegeneration remains unknown.</p><p><strong>Methods: </strong>Flow cytometry analysis was performed to examine MAIT cells in human Tau P301S transgenic mice. Tau pathology, hippocampus atrophy, meningeal integrity, and microglial gene expression were examined in Mr1^-/- P301S mice that lacked MAIT cells and control P301S transgenic mice, as well as Mr1^-/- P301S mice with adoptive transfer of MAIT cells.</p><p><strong>Results: </strong>The meninges of P301S mutant human tau transgenic mice had increased numbers of MAIT cells, which retained their expression of antioxidant molecules. Mr1^-/-P301S mice that lacked MAIT cells exhibited increased tau pathology and hippocampus atrophy compared to control Mr1^+/+P301S mice. Adoptive transfer of MAIT cells reduced tau pathology and hippocampus atrophy in Mr1^-/- P301S mice. Meningeal barrier integrity was compromised in Mr1^-/-P301S mice, but not in control Mr1^+/+P301S mice. A distinctive microglia subset with a proinflammatory gene expression profile (M-inflammatory) was enriched in the hippocampus of Mr1^-/-P301S mice. The transcriptomes of the remaining microglia in these mice also shifted towards a proinflammatory state, with increased expression of inflammatory cytokines, chemokines, and genes related to ribosome biogenesis and immune responses to toxic substances. The transfer of MAIT cells restored meningeal barrier integrity and suppressed microglial inflammation in the Mr1^-/- P301S mice.</p><p><strong>Conclusions: </strong>Our data indicate an important role for MAIT cells in regulating tau-pathology-related neuroinflammation and neurodegeneration.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"90"},"PeriodicalIF":9.3,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11927249/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}