International immunopharmacology最新文献

{"title":"Dexmedetomidine attenuates sepsis-associated acute lung injury by regulating macrophage efferocytosis through the ROS/ADAM10/AXL pathway.","authors":"Fei Li, Yan Bai, Zhu Guan, Xingyue Ji, Xinyu Zhan, Yiyun Gao, Weizhe Zhong, Zhuqing Rao","doi":"10.1016/j.intimp.2024.112832","DOIUrl":"10.1016/j.intimp.2024.112832","url":null,"abstract":"<p><strong>Background: </strong>The lungs are highly susceptible to damage during sepsis, with severe lung injury potentially progressing to acute respiratory distress syndrome and even fatal sepsis. Effective efferocytosis of apoptotic cells is crucial in alleviating inflammation and tissue injury.</p><p><strong>Methods: </strong>We established a septic lung injury mouse model via intraperitoneal injection of lipopolysaccharide. Lung injury was assessed by histology, immunofluorescence, neutrophil immunohistochemistry staining, and cytokine detection. We extracted alveolar macrophages by bronchoalveolar lavage and primary macrophages from mouse bone marrow to investigate the regulatory effects of Dexmedetomidine (DEX) on efferocytosis. We further validated the molecular mechanisms underlying the regulation of macrophage efferocytosis by DEX through knockdown of AXL expression. Additionally, we examined the efferocytic ability of monocytes isolated from patients.</p><p><strong>Results: </strong>We discovered that DEX treatment effectively alleviated pulmonary injury and inflammation. Lipopolysaccharide reduced macrophage efferocytosis and AXL expression which were reversed by DEX. We also found DEX inhibited the increased activation of A Disintegrin And Metalloproteinase 10 (ADAM10) and the production of soluble AXL. Moreover, our findings demonstrated that DEX decreased the elevated ROS production linked to higher ADAM10 activation. Blocking AXL negated DEX's benefits on efferocytosis and lung protection. Efferocytosis in monocytes from septic lung injury patients was notably lower than in healthy individuals.</p><p><strong>Conclusion: </strong>Our findings demonstrated that DEX treatment effectively reduces septic lung injury by promoting macrophage efferocytosis through ROS/ADAM10/AXL signaling pathwway.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":" ","pages":"112832"},"PeriodicalIF":4.8,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142371775","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":"The malic acid inhibiting inflammation in ankylosing spondylitis by interfering M1 macrophage polarization.","authors":"Zhou Ji, Xinzhe Feng, Changhao Han, Shuo Li, Bin Wu, Xuchao Zhang, Shanbang Zhu, Wenwen Tong, Weidong Xu","doi":"10.1016/j.intimp.2024.113653","DOIUrl":"https://doi.org/10.1016/j.intimp.2024.113653","url":null,"abstract":"<p><p>Ankylosing spondylitis (AS) is a motor system immune disease with significant genetic characteristics, resulting in joint fusion, deformity, rigidity, seriously affecting the quality of life of patients. Inflammatory bowel disease (IBD), characterized by intestinal mucosal damage and inflammatory changes, the most common extra-articular manifestation of AS. Due to the limitations of the application of therapeutic drugs, it is urgent to look for new mechanisms and strategies to effectively inhibit AS inflammation is. The content of malic acid (MA) was significantly decreased in peripheral blood of AS patients, and it was significantly negatively correlated with C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). MA dramatically alleviated spinal damage and intestinal inflammation in mouse models of AS induced by β-1, 3-glucan solution. Mechanically, MA suppressed the NF-κB pathway by inhibiting polarization of M1-type macrophages, thereby alleviating spinal and intestinal inflammation. From the perspective of material metabolism, this study explored the mechanism by which MA, an intermediate product of glucose metabolism, reducing M1 polarization of macrophages to inhibit AS inflammation, providing a reliable basis for the pathogenesis research and precise targeted treatment of AS in the later stage.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"144 ","pages":"113653"},"PeriodicalIF":4.8,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681766","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":"Role of macrophages in vascular calcification: From the perspective of homeostasis.","authors":"Rong Dong, Zhenjun Ji, Mi Wang, Genshan Ma","doi":"10.1016/j.intimp.2024.113635","DOIUrl":"https://doi.org/10.1016/j.intimp.2024.113635","url":null,"abstract":"<p><p>Vascular calcification (VC) is a crucial risk factor for the high morbidity and mortality associated with cardiovascular and cerebrovascular diseases. With the global population aging, the incidence of VC is escalating annually. However, due to its silent clinical process, VC often results in irreversible clinical outcomes. Inflammation is a core element in the VC process, and macrophages are the major inflammatory cells. Due to their diverse origins, microenvironments, and polarization states, macrophages exhibit significant heterogeneity, exerting strong effects on the occurrence, development, and even the regression of VC. In this review, we summarize the origin, distribution, classification, and surface markers of macrophages. Simultaneously, we explore the mechanisms by which macrophages maintain homeostasis or regulate inflammation, including the macrophage-mediated regulation of VC through the release of inflammatory factors, osteogenic genes, extracellular vesicles, and alterations in efferocytosis. Finally, we discuss research targeting inflammation and macrophages to develop novel therapeutic regimens for preventing and treating VC.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"144 ","pages":"113635"},"PeriodicalIF":4.8,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681740","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":"High-density lipoprotein alleviates ocular inflammation by downregulating M1 microglia and pyroptosis through regulating lipid accumulation and Caveolin-1 expression.","authors":"Enguang Chen, Han Chen, Yuan Yang, Miaomiao Liu, Jianhui Wang, Xuerui Zhang, Haodong Xiao, Jing Li, Huazhang Feng, Yu Xu","doi":"10.1016/j.intimp.2024.113592","DOIUrl":"https://doi.org/10.1016/j.intimp.2024.113592","url":null,"abstract":"<p><p>Uveitis encompasses a group of intraocular inflammatory diseases that are often associated with low levels of high-density lipoprotein (HDL). The role of HDL in intraocular inflammatory diseases remains unclear. In our research, we established an endotoxin-induced uveitis (EIU) model to investigate the role of HDL. Our study indicated that HDL could suppress ocular inflammation and restore retinal function in EIU mice. Specifically, HDL intervention effectively inhibited microglial activation and promoted the transformation of microglia from the M1 phenotype to the M2 phenotype. Furthermore, HDL intervention reduced microglial pyroptosis. Additionally, HDL was found to inhibit lipid accumulation in LPS-induced microglia, which is associated with inflammation, M1 polarization, and pyroptosis, by enhancing the expression of Caveolin-1 (CAV-1). Finally, we demonstrated that the function of HDL may be partially dependent on CAV-1 expression. We conclude that HDL inhibits pathological ocular inflammation by regulating M1/M2 phenotype polarization and pyroptosis through the modulation of lipid accumulation and CAV-1 expression. This suggests that HDL may represent a novel therapeutic strategy for ocular inflammation.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"144 ","pages":"113592"},"PeriodicalIF":4.8,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681694","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":"The efficacy and active compounds of Chaihuang Qingyi Huoxue granule to Ameliorate intestinal mucosal barrier injury in rats with severe acute pancreatitis by suppressing the HMGB1/TLR4/NF-κB signaling pathway.","authors":"Jian-Qin Liu, Wei-An Hao, Ya-Li Liu, Dan Yang, Hong-Lian Wang, Long Zhao, Hui Chen, Li Li, Chao-Li Jiang, Xin Zhou, Juan Fu, Zhi Li","doi":"10.1016/j.intimp.2024.113632","DOIUrl":"https://doi.org/10.1016/j.intimp.2024.113632","url":null,"abstract":"<p><p>Intestinal mucosal barrier injury represents a critical complication of severe acute pancreatitis (SAP) without effective treatment. This study investigated the efficacy, underlying mechanism, and responsible active compounds of the traditional Chinese medicinal prescription Chaihuang Qingyi Huoxue granule (CHQY) in treating SAP-induced intestinal mucosal barrier injury. SAP was established in Sprague-Dawley rats via intra-pancreaticobiliary duct infusion of sodium taurocholate, followed by oral CHQY administration (3.15 g/kg every 6 h for 12 and 24 h). Blood and tissues were harvested to assess the severity of pancreatitis, intestinal mucosal barrier integrity, and extent of inflammatory injury. Intestine-absorbing compounds were identified using ultra-high-performance liquid chromatography coupled with high-resolution mass spectrometry (UHPLC-HRMS). Our results showed that CHQY treatment effectively mitigated SAP-induced intestinal mucosal injury, as evidenced by improved intestinal epithelial structure, decreased serum levels of intestinal injury markers (d-lactic acid, diamine oxidase, I-FABP, and Zonulin), restored expression of the tight junction protein ZO-1, and reduced serum endotoxin levels. Furthermore, CHQY administration suppressed the expression of proinflammatory mediator HMGB1, its receptor TLR4, and downstream NF-κB signaling in the intestine, leading to downregulated intestinal IL-1β expression and reduced circulating TNF-α and IL-6. UHPLC-HRMS analysis identified 15 intestine-absorbing compounds in CHQY, of which paeoniflorin sulfite and chrysin-7-O-glucuronide independently inhibited TNF-α-induced tight junction loss in IEC-6 cells and mitigated intestinal mucosal barrier injury in SAP rats through suppressing NF-κB signaling. In summary, CHQY ameliorates SAP-induced intestinal mucosal barrier injury by downregulating the proinflammatory HMGB1/TLR4/NF-κB signaling, with efficacy partially attributed to its active compounds paeoniflorin sulfite and chrysin-7-O-glucuronide.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"144 ","pages":"113632"},"PeriodicalIF":4.8,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681763","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":"ANP32E promotes esophageal cancer progression and paclitaxel resistance via P53/SLC7A11 axis-regulated ferroptosis.","authors":"Li-Ying Sun, Shao-Bo Ke, Bo-Xin Li, Fei-Shan Chen, Zhi-Qun Huang, Le Li, Jian-Feng Zhang, Yu-Xin Cai, Hang-Jia Zhu, Xiao-Dong Zhang, Run-Lei Du, Yi Liu, Yong-Shun Chen","doi":"10.1016/j.intimp.2024.113436","DOIUrl":"https://doi.org/10.1016/j.intimp.2024.113436","url":null,"abstract":"<p><p>Esophageal cancer (EC) is associated with high mortality rates and widespread resistance to chemotherapeutic agents, like paclitaxel (PTX), posing a significant global public health challenge. ANP32E is a member of the acidic nuclear phosphoprotein 32 family, its specific biological functions and mechanisms in EC remain unclear. Through bioinformatics analysis and clinical tissue sample studies, we observed a marked upregulation of ANP32E expression in EC tissues. Utilizing ANP32E knock-out EC cell models and xenograft experiments in nude mice, we demonstrated that the absence of ANP32E significantly inhibits tumor progression and migration, whereas its overexpression exacerbates tumor growth. Transcriptomic sequencing (RNA-seq) further revealed activation of the ferroptosis pathway in ANP32E deficient cells, which was confirmed through experiments showing enhanced ferroptosis that could be reversed by the ferroptosis inhibitor ferrostatin-1. At the molecular level, ANP32E regulates EC progression and ferroptosis via the p53/SLC7A11 axis. ANP32E depletion resulted in increased p53 expression level, while inhibition of p53 partially restored the suppressed cell proliferation and increased ferroptosis in ANP32E-depleted cells. Additionally, knocking out ANP32E significantly enhanced EC cell sensitivity to PTX, Combining PTX with the ferroptosis inducer erastin was more effective in inhibiting tumor growth. In vivo, we confirmed the synergistic effect of ANP32E knock-out combined with PTX demonstrating superior tumor suppressing. Overall, our findings suggest that ANP32E regulates EC progression and ferroptosis through the p53/SLC7A11 axis, offering a potential molecular target for overcoming PTX resistance in EC treatment.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"144 ","pages":"113436"},"PeriodicalIF":4.8,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681692","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":"Potential and limitations of IL-37, a cytokine targeted for therapy of systemic lupus erythematosus: A Systematic Review.","authors":"Ummul Aqeela Balqees Mohamed Thaha, Wan Majdiah Wan Mohamad, Nik Rosmawati Nik Husain, Norhayati Yusop, Rohimah Mohamud, Wan Syamimee Wan Ghazali","doi":"10.1016/j.intimp.2024.113597","DOIUrl":"https://doi.org/10.1016/j.intimp.2024.113597","url":null,"abstract":"<p><strong>Background: </strong>Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by dysregulated immune responses and inflammation. Interleukin-37 (IL-37) is a recently discovered immunomodulatory cytokine with potential anti-inflammatory properties. This systematic review explores the relationship between IL and 37 and SLE disease activity, and evaluates its potential as a therapeutic agent.</p><p><strong>Methods: </strong>Electronic databases were searched for studies investigating IL-37 and SLE. Data on IL-37 levels, SLE Disease Activity Index (SLEDAI) score, genetic polymorphisms, and its therapeutic effects from pre-clinical studies were extracted.</p><p><strong>Results: </strong>Previous studies presented conflicting findings on IL-37 levels in SLE patients. Some reported positive correlations with disease activity, while others observed associations between lower IL-37 and increased activity. Genetic variations in the IL-37 gene linked to SLE susceptibility have been reported. Pre-clinical studies using engineered mesenchymal stem cells or direct IL-37 treatment showed promise in reducing disease severity in mouse models and cell cultures of SLE. The analysis of multiple studies reveals that IL-37 expression varies significantly across different SLE subtypes.</p><p><strong>Conclusions: </strong>While a potential link exists between IL and 37 and disease activity, genetic predisposition, and therapeutic benefit, further research is needed. Future studies with standardized designs, larger and more diverse populations, and mechanistic investigations are crucial to determine the therapeutic potential of IL-37 for SLE. This review highlights the need for well-designed clinical trials to evaluate the safety and efficacy of IL-37 therapy in patients with SLE.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"144 ","pages":"113597"},"PeriodicalIF":4.8,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681736","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":"Novel therapeutic targets for atherosclerosis: Targeting the FOSB-MECP2-Commd1 pathway.","authors":"Xi Fu, Changlu Xu, Tiangui Yang, Jie Chen, Tiesheng Niu","doi":"10.1016/j.intimp.2024.113575","DOIUrl":"https://doi.org/10.1016/j.intimp.2024.113575","url":null,"abstract":"<p><p>Atherosclerosis (AS) is a systemic disease and represents the primary underlying pathology of cardiovascular diseases. In this study, we aim to elucidate the roles of FBJ osteosarcoma oncogene B (FOSB) in AS development. ApoE^-/- mice were used and fed a high-fat diet to establish an AS model. We observed elevated expression of FOSB in aortic tissues, which was associated with increased lipid deposition, macrophage recruitment. Knockdown of FOSB mitigated these AS-related pathological changes, and decreased the levels of TNF-α, IL-6 and IL-1β in aortic tissues and ox-LDL-induced RAW264.7 cells. Further investigations revealed that FOSB enhances the transcriptional activity of MECP2 by binding to its promoter region. MECP2 was found to be upregulated in aortic tissues and ox-LDL-induced RAW264.7 cells, exacerbating ox-LDL-induced cellular damage. Additionally, our study identifies Commd1 as a downstream target of MECP2. Overexpression of Commd1 reduced levels of TNF-α and IL-6, alleviating ox-LDL-induced inflammation and lipid deposition. In summary, our findings unveil a complex molecular interplay involving FOSB, MECP2, and Commd1 in AS pathogenesis. This study not only enhances our understanding of AS molecular mechanisms but also proposes potential therapeutic targets for its treatment.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"144 ","pages":"113575"},"PeriodicalIF":4.8,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681672","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":"The effector protein BspE affects Brucella survival by regulating the inflammatory response and apoptosis.","authors":"Jinke He, Shuanghong Yin, Xiaoyu Deng, Zhongchen Ma, Huan Zhang, Yuhe Miao, Jihai Yi, Chuangfu Chen, Junbo Zhang","doi":"10.1016/j.intimp.2024.113576","DOIUrl":"https://doi.org/10.1016/j.intimp.2024.113576","url":null,"abstract":"<p><p>Brucella T4SS secretes numerous effector proteins to disrupt host immune responses and apoptosis, enabling long-term survival. One such effector protein is BspE, whose role remains largely unknown. In this study, we demonstrated that BspE promotes the growth of Brucella, enhances its survival in macrophages, and affects the release of macrophage inflammatory factors. Furthermore, BspE facilitates Brucella colonization and pathological damage in mice. Our findings reveal that BspE can be translated in the host cell nucleus, where it interacts with the host RNA-binding protein PCBP1 to promote Brucella replication in macrophages. Knockdown of PCBP1 affects BspE-mediated proliferation of Brucella in macrophages. Furthermore, the BspE-PCBP1 interaction hinders P53 signaling and inhibits macrophage apoptosis. Although this interaction affects inflammatory cytokines, it does not significantly involve the NF-κB pathway. These findings contribute to a better understanding of how the Brucella effector protein BspE regulates host immune responses and apoptosis to influence its own survival.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"144 ","pages":"113576"},"PeriodicalIF":4.8,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681760","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":"Molecular signaling pathways in doxorubicin-induced nephrotoxicity and potential therapeutic agents.","authors":"Changxu Lu, Jinwen Wei, Can Gao, Mingli Sun, Dan Dong, Zhongyi Mu","doi":"10.1016/j.intimp.2024.113373","DOIUrl":"https://doi.org/10.1016/j.intimp.2024.113373","url":null,"abstract":"<p><p>Doxorubicin (DOX), an anthracycline chemotherapeutic agent, is extensively utilized in the clinical management of both solid and hematological malignancies. Nevertheless, the clinical application of this treatment is significantly limited by adverse reactions and toxicity that may arise during or after administration. Its cytotoxic effects are multifaceted, with cardiotoxicity being the most prevalent side effect. Furthermore, it has the potential to adversely affect other organs, including the brain, kidneys, liver, and so on. Notably, it has been reported that DOX may cause renal failure in patients and there is currently no effective treatment for DOX-induced kidney damage, which has raised a high concern about DOX-induced nephrotoxicity (DIN). Although the precise molecular mechanisms underlying DIN remain incompletely elucidated, prior research has indicated that reactive oxygen species (ROS) are pivotal in this process, triggering a cascade of detrimental pathways including apoptosis, inflammation, dysregulated autophagic flux, and fibrosis. In light of these mechanisms, decades of research have uncovered several DIN-associated signaling pathways and found multiple potential therapeutic agents targeting them. Thus, this review intends to delineate the DIN associated signaling pathways, including AMPK, JAKs/STATs, TRPC6/RhoA/ROCK1, YAP/TEAD, SIRTs, Wnt/β-catenin, TGF-β/Smad, MAPK, Nrf2/ARE, NF-κB, and PI3K/AKT, and to summarize their potential regulatory agents, which provide a reference for the development of novel medicines against DIN.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"144 ","pages":"113373"},"PeriodicalIF":4.8,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681707","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}