Genes and immunity最新文献

{"title":"STAMBP drives colorectal cancer progression via CXCR4 deubiquitination and bone marrow-derived suppressor cell recruitment","authors":"Yang Yang, Song Zhao, Feng Jing, Zihan Xiong, Mei Li, Jing Xia","doi":"10.1038/s41435-026-00375-5","DOIUrl":"10.1038/s41435-026-00375-5","url":null,"abstract":"Colorectal cancer (CRC) is one of the three leading causes of tumor-related mortality worldwide. The recruitment of bone marrow-derived suppressor cells (MDSCs) is a key mechanism by which tumors evade immune surveillance, as these cells inhibit T cell activity and accelerate CRC progression. STAMBP, a member of the Jab1/MPN metalloenzyme family of deubiquitinases (DUBs), cleaves K63-linked polyubiquitin chains from protein substrates and participates in diverse physiological and pathological processes. Nevertheless, its role in CRC and the mechanisms through which it contributes to disease progression have not been clearly defined. In the present study, we observed that both STAMBP and MDSCs were significantly upregulated in CRC tissues and cell lines. Functional assays revealed that STAMBP promotes CRC cell proliferation while simultaneously enhancing MDSC recruitment. Mechanistic analysis demonstrated that STAMBP regulates the deubiquitination of CXCR4, which stabilizes its protein expression. Silencing of CXCR4 not only suppressed CRC cell growth but also diminished MDSC infiltration. In conclusion, these findings indicate that STAMBP facilitates CRC progression through CXCR4 stabilization and MDSCs recruitment, highlighting a potential target for therapeutic intervention.","PeriodicalId":12691,"journal":{"name":"Genes and immunity","volume":"27 2","pages":"173-184"},"PeriodicalIF":4.5,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146010040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"m6A RNA methylation modulates antiviral response in celiac disease","authors":"Maialen Sebastian-delaCruz, Ane Olazagoitia-Garmendia, Izei Pascual-Gonzalez, Luis Manuel Mendoza, Maria Legarda, Carlos Tutau, Luis Bujanda, Sankar Ghosh, Izortze Santin, Thomas S. Postler, Jose Ramon Bilbao, Ainara Castellanos-Rubio","doi":"10.1038/s41435-025-00373-z","DOIUrl":"10.1038/s41435-025-00373-z","url":null,"abstract":"N6-methyladenosine (m6A) RNA modifications and reovirus infections have recently been implicated in the development of celiac disease. While viral infections are known to alter the RNA modification machinery of the host, their interplay in autoimmune tissue damage remains unexplored. In this study we employed an in vitro model combining a viral mimic with gliadin peptides to simulate celiac disease conditions, alongside the analysis of serum and intestinal biopsies from controls and patients to investigate the link between m6A methylation and viral infections in inducing autoimmune inflammation. We found elevated anti-reovirus reactivity in patients, increased antiviral gene expression and enhanced m6A levels. Notably, the expression of IRF7 was synergistically induced by the combined exposure to the viral mimic and gliadin peptides, and this is mediated through m6A methylation in its coding region and interaction with the reader protein YTHDC2. Furthermore, the reduction of m6A through METTL3 silencing or simvastatin treatment reduced IRF7 mRNA methylation and downstream proinflammatory gene expression both in vitro and ex vivo. These findings highlight m6A methylation as a modulator of antiviral responses and a potential therapeutic target in autoimmune disorders.","PeriodicalId":12691,"journal":{"name":"Genes and immunity","volume":"27 1","pages":"130-139"},"PeriodicalIF":4.5,"publicationDate":"2026-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41435-025-00373-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145943198","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":"Recruitment of CCR5+ inflammatory monocytes in pulmonary tissue contributes to acute lung injury","authors":"Dongdong Wei, Xuebiao Li, Guocong Xu, Yupeng Sun, Xian Zhu, Qunjun Duan, Ning Gao, Aiqiang Dong, Minjian Kong","doi":"10.1038/s41435-025-00371-1","DOIUrl":"10.1038/s41435-025-00371-1","url":null,"abstract":"Acute lung injury (ALI) is a common serious complication following deep hypothermic circulatory arrest (DHCA). Monocytes and macrophages play crucial roles in producing inflammatory mediators and regulating innate and adaptive immunity. In our specific rat model of DHCA-induced ALI, we previously showed that autophagy actually has a detrimental effect on lung injury rather than a protective effect. Recently, we reported that monocytes serve an important role in this model. Here, single-cell RNA sequencing was performed on lung tissue cells collected from healthy rats and rats after DHCA. Notably, there was a selective and dramatic increase in the subpopulation of CD43low monocytes in the DHCA group, which expressed high levels of CCR5 and exhibited a proinflammatory phenotype. Allosteric CCR5 drug blockade not only reduced CCR5 expression and alleviated lung injury but also, interestingly, inhibited autophagy. These results suggest that the recruitment of CCR5+ inflammatory monocytes into pulmonary tissue contributes to ALI after DHCA and that blocking CCR5 is a plausible intervention for DHCA-induced lung injury by modulating autophagy.","PeriodicalId":12691,"journal":{"name":"Genes and immunity","volume":"27 1","pages":"106-116"},"PeriodicalIF":4.5,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41435-025-00371-1.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145827393","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":"Radiotherapy combined with anti-PD-1 immunotherapy promotes ferroptosis-driven control of hepatocellular carcinoma","authors":"Ting Dou, Xianggao Zhu, Hong Li, Runmei Wang, Jiepu He, Hongwei Geng, Wei Zhang, Qin Yu, Haiping Zhao, Hao Yang","doi":"10.1038/s41435-025-00370-2","DOIUrl":"10.1038/s41435-025-00370-2","url":null,"abstract":"Combination of radiotherapy (RT) and anti-PD-1 immunotherapy (IO) has shown significant efficacy in treating hepatocellular carcinoma (HCC). Nevertheless, yet the underlying mechanisms remain incompletely understood. A Hepa1-6 mouse HCC model was established to explore the anti-tumor mechanism of combination therapy in HCC. Notably, combination therapy effectively inhibited tumor growth in mice bearing Hepa1-6 tumors. Through MeRIP-sequencing, we indicated that combination therapy increased m6A modification and reduced mRNA expression of Hspb1, a negative regulator of ferroptosis, in tumors from mice. Both combination therapy and Hspb1 downregulation significantly induced Hepa1-6 cell ferroptosis. Metabolomics analysis revealed that Hspb1 downregulation further promoted abnormal lipid metabolism in Hepa1-6 tumor-bearing mice, enhancing pro-ferroptosis effects of combination therapy. Meanwhile, Hspb1 downregulation further enhanced RT and IO-induced anti-tumor immune response in tumor-bearing mice, as evidenced by significantly elevated numbers of cytotoxic CD8 + T cells. Additionally, combination therapy also significantly downregulated RNA demethylase Alkbh5 in tumor-bearing mice. Overexpression of Alkbh5 increased Hspb1 expression and inhibited ferroptosis, indicating that Alkbh5 regulates ferroptosis through targeting Hspb1. Targeting Alkbh5/Hspb1/ferroptosis axis may enhance anti-tumor effects in combination therapy, highlighting a potential therapeutic approach for HCC.","PeriodicalId":12691,"journal":{"name":"Genes and immunity","volume":"27 1","pages":"91-105"},"PeriodicalIF":4.5,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41435-025-00370-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145781007","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":"Structural and functional analysis of the TGF-β mimic, TGM-2: an immunomodulatory helminth protein","authors":"Emmaculate Yaah Ntang, Kyle T. Cunningham, Shashi P. Singh, Claire Ciancia, Anna Sanders, Sergio Lilla, Ananya Mukundan, Stephen M. Ghogomu, Andrew P. Hinck, Rick M. Maizels","doi":"10.1038/s41435-025-00372-0","DOIUrl":"10.1038/s41435-025-00372-0","url":null,"abstract":"The extraordinary prevalence of helminths is attributable to secretion of molecules that manipulate the host immune system, facilitating their survival. Among the secretory products of the murine intestinal helminth Heligmosomoides polygyrus are 10 mimic proteins with functional resemblance to the mammalian immunosuppressive cytokine, TGF-β, but structurally distinct with five Complement Control Protein (CCP) domains, designated TGM-1 to −10. Here we dissect the structure and function of the mimic TGM-2 and its domains. We generated eight protein truncations lacking N- or C-terminal domains, for testing through pulldowns, mass spectrometric analysis and isothermal titration calorimetry, confirming affinity for TGFBR1 (ALK5), TGFBR2, and the co-receptor CD44. We observed that domains 1–3 bind TGFBR1 and TGFBR2, while domains 4 and 5 exhibit stronger binding to the CD44 co-receptor than TGM-1. Additionally, full-length TGM-2 activates the pSMAD pathway in the MFB-F11 fibroblast cell line at concentrations as low as 1 ng/mL and induces the in vitro conversion of naïve murine CD4+ T cells into Foxp3+ Tregs. Both stimulatory activities diminish significantly in the absence of domains 4 and 5 that interact with CD44. In vivo, both full-length TGM-2 and truncated Domains 1–3 construct potently alleviate allergic airway inflammation in mice exposed to Alternaria alternata allergen.","PeriodicalId":12691,"journal":{"name":"Genes and immunity","volume":"27 1","pages":"117-129"},"PeriodicalIF":4.5,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41435-025-00372-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145780962","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":"Molecular analysis and immunological characterization of a founder mutation causing ARPC1B deficiency","authors":"Megan M. Dobrose, Meltem Ece Kars, Jareb J. Perez-Caraballo, Colleen M. Roark, Christine Mariskanish, Oscar Zavaleta-Martinez, Noemi Gomez-Hernandez, Saul Oswaldo Lugo-Reyes, Yuval Itan, Lizbeth Blancas-Galicia, Rubén Martínez-Barricarte","doi":"10.1038/s41435-025-00368-w","DOIUrl":"10.1038/s41435-025-00368-w","url":null,"abstract":"Actin-Related Protein Complex 1B (ARPC1B) is a subunit of the ARP2/3 complex that is predominately expressed in hematopoietic cells and is involved in the regulation of actin polymerization. ARPC1B deficiency leads to combined immunodeficiency (CID) with symptoms of eczema, allergies, inflammation, recurrent infection, and thrombocytopenia. We characterize the disease-causing variant c.899_944del (p.E300Gfs*7) on the ARPC1B gene that originated from a founder effect in an indigenous American population. We showed that this variant impairs protein expression leading to a complete deficiency of ARPC1B. Additionally, we used mass cytometry to thoroughly analyze the effects of this mutation on the frequencies of immune populations. Our findings suggest that ARPC1B is critical for class switching since our ARPC1B-deficient patient had reduced frequencies of class-switched memory B cells. Furthermore, the frequencies of total CD4+, CD8+, and γδ T cells were reduced, consistent with an essential function of ARPC1B in T cell development. Overall, this study advances the knowledge of the c.899_944del ARPC1B mutation and the understanding of the role of ARPC1B in the immune system.","PeriodicalId":12691,"journal":{"name":"Genes and immunity","volume":"27 1","pages":"69-80"},"PeriodicalIF":4.5,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41435-025-00368-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145540153","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":"Spatiotemporal transcriptomic insights into ferroptosis and TFRC-linked immune interactions in ischemia-reperfusion acute kidney injury","authors":"Yulin Wang, Cheng Zhu, Shiqi Lv, Xinhui Huang, Jiayi Wang, Shuangxin Yuan, Yue Yang, Xiaoqiang Ding, Ziyan Shen, Xiaoyan Zhang","doi":"10.1038/s41435-025-00364-0","DOIUrl":"10.1038/s41435-025-00364-0","url":null,"abstract":"Acute kidney injury (AKI) is a common and critical clinical condition with complex pathogenesis and limited early intervention options. Ferroptosis, an iron-dependent form of cell death driven by lipid peroxidation, plays a pivotal role in AKI development. This study aimed to investigate ferroptosis-related gene expression, spatial distribution, and immune interactions in AKI to identify potential therapeutic targets. We analyzed gene expression changes in a mouse model of ischemia–reperfusion-induced AKI and constructed a machine learning–based diagnostic model. This model identified five ferroptosis-related genes (TFRC, TXNRD1, SLC39A14, GCLM, and HMOX1) closely associated with immune cell infiltration. Integration of single-cell and spatial transcriptomics revealed that these genes were predominantly expressed in proximal tubule cells. Notably, TFRC exhibited distinct spatial proximity to infiltrating macrophages. In vivo, administration of the ferroptosis inhibitor NSC306711 significantly reduced macrophage infiltration and renal injury, as confirmed by immunofluorescence. In vitro, co-culture experiments showed that TfR1 degradation alleviated hypoxia–reoxygenation injury in tubular cells and attenuated immune cell activation. This study highlights the central role of ferroptosis in AKI pathogenesis and its interaction with immune components in the renal microenvironment. Targeting ferroptosis, particularly TFRC, may offer a promising strategy to mitigate kidney injury and immune activation in AKI.","PeriodicalId":12691,"journal":{"name":"Genes and immunity","volume":"27 1","pages":"25-40"},"PeriodicalIF":4.5,"publicationDate":"2025-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41435-025-00364-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145530665","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":"Macrophage retrotransposon expression is associated with lupus","authors":"Jianghong Zhong, Zhongheng Chen, Hangqi Yue, Zhicheng Han, Weibin Zhu","doi":"10.1038/s41435-025-00369-9","DOIUrl":"10.1038/s41435-025-00369-9","url":null,"abstract":"Genetic variants of NCF1 that impair the production of reactive oxygen species (ROS) are associated with lupus in humans; however, the underlying mechanism of immune dysregulation remains unclear. To clarify this mechanism, the study tested the hypothesis that retrotransposons contribute to the early onset of lupus by facilitating the expansion and activation of macrophages. Using the ROS-deficient lupus-prone lpr mouse model, we employed bulk RNA sequencing, flow cytometry, and spatially resolved single-cell transcriptome imaging to comprehensively characterize tissue-resident macrophages. The results demonstrated increased expression of the mouse transcript family type D (MTD) retrotransposon in tissue-resident macrophages from the spleen, kidneys, and skull dura of ROS-deficient lpr mice, indicating a link between ROS deficiency, MTD expression, and macrophage expansion. Importantly, this MTD expression decreased following two weeks of mycophenolate mofetil therapy, linking therapy response to retrotransposon activity. Furthermore, the MTD-encoded RNA was used to disrupt the signaling of retrotransposons, leading to regulatory T-cell activation and downregulation of both glomerular macrophage infiltration and serum interleukin-6 secretion in lupus-prone mice. Collectively, these findings suggest that the MTD retrotransposons play a crucial role in driving the early onset of lupus by enhancing macrophage activation, which in turn promotes immune dysregulation.","PeriodicalId":12691,"journal":{"name":"Genes and immunity","volume":"27 1","pages":"81-90"},"PeriodicalIF":4.5,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145512553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"YTHDF1 mediates KLF2/VSIG4 axis to regulate Kupffer cell polarization to alleviate sepsis-induced liver injury","authors":"Na Sun, Yunhai Wu, Bin Liu, Peihua Xu, Guoqiang Shen, Jinlong Li, Chonghao Ma, Zongxuan Zhang","doi":"10.1038/s41435-025-00367-x","DOIUrl":"10.1038/s41435-025-00367-x","url":null,"abstract":"The severity and prognosis of sepsis patients are directly linked to liver damage. Encouraging Kupffer cell transition from M1 to M2 can notably diminish inflammation and hepatic damage triggered by sepsis. Here, the effect of YTH domain N6-methyladenosine RNA binding protein F1 (YTHDF1) on Kupffer cell polarization in sepsis was evaluated. Histological staining of liver sections was conducted in CLP mice. Macrophage markers (M1:iNOS; M2:Arg1) and hepatocyte apoptosis were measured using flow cytometry. Western blot measured protein levels of YTHDF1, KLF2, VSIG4 and macrophage polarization markers. Interactions between YTHDF1, KLF2 and VSIG4 were explored by ChIP, RIP and dual luciferase reporter assays. We found that, in patients with sepsis-induced liver injury and LPS-stimulated macrophages, KLF2 and VSIG4 expression was reduced. KLF2 upregulation facilitated VSIG4 transcriptional regulation in Kupffer cells, promoting M2 polarization to alleviate hepatocyte injury triggered by LPS. The m6A level of KLF2 was regulated by YTHDF1, influencing KLF2 translation. YTHDF1 elevated KLF2 levels, fostering Kupffer M2 polarization to alleviate hepatocyte injury induced by LPS. YTHDF1 or KLF2 upregulation regulated Kupffer cell polarization, mitigating CLP-induced liver injury in septic mice. In conclusion, YTHDF1 reduced sepsis-induced inflammatory responses and liver damage by enhancing Kupffer cell M2 polarization through KLF2/VSIG4 pathway.","PeriodicalId":12691,"journal":{"name":"Genes and immunity","volume":"27 1","pages":"58-68"},"PeriodicalIF":4.5,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145458384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of nucleic acid metabolism on prognosis and immune invasion of triple-negative breast cancer","authors":"Fan Yang, Yin Dong, Siqi Wu, Yanting You, Ying Yang, Jingwei Kong, Jie Chen, Liqian Chen, Xuefeng Jiang, Hiu Yee Kwan, Xiaoshan Zhao, Ji Wang, Yanyan Liu","doi":"10.1038/s41435-025-00366-y","DOIUrl":"10.1038/s41435-025-00366-y","url":null,"abstract":"The nucleic acid metabolism process is driven by various carcinogenic factors, providing a material basis and energy guarantee for the malignant phenotype of tumor cells. However, the role of nucleic acid metabolism in triple-negative breast cancer (TNBC) development remains unclear. Here, we examined the expression patterns of nucleic acid metabolism-related genes (NAMRGs) in the transcriptome of 297 TNBC samples derived from three datasets. We used single-cell RNA sequencing analysis and both in vivo and in vitro experiments to verify the correlation between NAMRGs and tumor metastasis and tumor immune matrix microenvironment (TME) characteristics. According to the results, two different molecular subtypes were identified, and the relationships between the molecular subtypes, four genetic subtypes, and four pathological subtypes were established. Changes in nucleic acid metabolism were related to changes in homologous recombination repair defects (HRD), cell infiltration in the TME, and patient prognosis. We also constructed a prediction model, NAM_model, by including four NAMRGs (DPYD, PDE6G, PDE8B, and TYMS) and integrating it with other clinical indicators. This model was a highly accurate prognostic nomogram, which showed that the prognosis of high-risk patients was poor, with NAMRGs associated with TME immune exhaustion. In addition, NAMRGs were significantly correlated with drug sensitivity to chemotherapy and targeted therapy. In vivo and in vitro studies have shown that PDE8B is an oncogene that promotes tumor growth and induces TNBC metastasis by promoting epithelial-mesenchymal transition (EMT), which has not been reported previously. Single-cell RNA sequencing also revealed the unique effects of nucleic acid metabolism and HRD on exhausted CD8+ T cells. A comprehensive analysis of NAMRGs revealed the potential impact of nucleic acid metabolism-mediated mechanisms, such as HRD and EMT, on the clinical pathological characteristics, TME characteristics, and prognosis of patients with TNBC. These findings have deepened our understanding of the roles of NAMRGs in TNBC and immunotherapy, which will greatly contribute to patient stratification management and individualized clinical decision-making.","PeriodicalId":12691,"journal":{"name":"Genes and immunity","volume":"27 1","pages":"41-57"},"PeriodicalIF":4.5,"publicationDate":"2025-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145458364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}