Signal Transduction and Targeted Therapy最新文献

{"title":"Bat organoid platform: revolutionizing zoonotic virus research and pandemic preparedness.","authors":"Young-Ho Park,Sun-Uk Kim,Taeho Kwon","doi":"10.1038/s41392-025-02323-7","DOIUrl":"https://doi.org/10.1038/s41392-025-02323-7","url":null,"abstract":"","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"8 1","pages":"224"},"PeriodicalIF":39.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144640010","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":"Dual-immunotherapy triumphs: redefining deficient mismatch repair or high microsatellite instability metastatic colorectal cancer first-line treatment","authors":"Zhijun Yuan, Saimeng Shi, Shanshan Weng","doi":"10.1038/s41392-025-02322-8","DOIUrl":"https://doi.org/10.1038/s41392-025-02322-8","url":null,"abstract":"<p>In a recent paper published in <i>Lancet</i> by Thierry Andre et al., CheckMate 8HW (NCT04008030) revealed that dual-agent immunotherapy improved the prognosis of deficient mismatch repair or high microsatellite instability (dMMR/MSI-H) metastatic colorectal cancer (mCRC) significantly.¹ The results emphasize the significant therapeutic advantages of combining nivolumab (programmed death-1 inhibitor) and ipilimumab (cytotoxic T-lymphocyte-associated antigen-4 inhibitor) in treating dMMR/MSI-H mCRC, irrespective of comparison with chemotherapy (first-line) or nivolumab monotherapy (all treatment lines).</p>","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"23 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144629764","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":"High mtDNA content identifies oxidative phosphorylation-driven acute myeloid leukemias and represents a therapeutic vulnerability.","authors":"Diego A Pereira-Martins,Isabel Weinhäuser,Emmanuel Griessinger,Juan L Coelho-Silva,Douglas R Silveira,Dominique Sternadt,Ayşegül Erdem,Bruno Kosa L Duarte,Prodromos Chatzikyriakou,Lynn Quek,Antonio Bruno Alves-Silva,Fabiola Traina,Sara T Olalla Saad,Jacobien R Hilberink,Amanda Moreira-Aguiar,Maria L Salustiano-Bandeira,Marinus M Lima,Pedro L Franca-Neto,Marcos A Bezerra,Nisha K van der Meer,Emanuele Ammatuna,Eduardo M Rego,Gerwin Huls,Jan Jacob Schuringa,Antonio R Lucena-Araujo","doi":"10.1038/s41392-025-02303-x","DOIUrl":"https://doi.org/10.1038/s41392-025-02303-x","url":null,"abstract":"Metabolic reprogramming is a hallmark of cancer, with acute myeloid leukemia (AML) being no exception. Mitochondrial function, particularly its role in protecting tumor cells against chemotherapy, is of significant interest in AML chemoresistance. In this study, we identified mitochondrial DNA content (mtDNAc), measured by quantitative PCR, as a simple and precise marker to stratify the metabolic states of AML patients. We show that patients with high mtDNAc are associated with increased mitochondrial metabolism and a higher dependency on oxidative phosphorylation (OXPHOS), often correlating with chemoresistance. Clinically, patients receiving cytarabine and an anthracycline-based regimen (7 + 3 regimen) experienced inferior relapse-free survival and a higher overall rate of leukemia recurrence. Ex vivo experiments using primary AML samples confirmed cytarabine resistance in high mtDNAc patients, which could be overcome by inhibiting mitochondrial complex I. The FDA-approved drug metformin, which targets mitochondrial metabolism, significantly enhanced apoptosis in response to chemotherapy or targeted agents, such as venetoclax, in AML models. However, metformin-treated cells adapted by increasing glycolysis and NAD+ production, a resistance mechanism that could be bypassed by targeting the nicotinamide phosphoribosyltransferase (NAMPT) enzyme. In summary, we demonstrated that mtDNAc is an effective tool for assessing the metabolic state of AML cells. This method can be easily implemented in clinical practice to identify chemoresistant patients and guide personalized treatment strategies, including novel combination therapies for those with a high reliance on mitochondrial metabolism.","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"7 1","pages":"222"},"PeriodicalIF":39.3,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144622110","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":"Pattern recognition receptors: function, regulation and therapeutic potential","authors":"Ruochan Chen, Ju Zou, Jiawang Chen, Xiao Zhong, Rui Kang, Daolin Tang","doi":"10.1038/s41392-025-02264-1","DOIUrl":"https://doi.org/10.1038/s41392-025-02264-1","url":null,"abstract":"<p>Pattern recognition receptors (PRRs) are sensors in the immune system, detecting pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). They serve as essential links between the innate and adaptive immune responses, initiating defense mechanisms against pathogens and maintaining immune homeostasis. This review examines the classification, structure, and signaling cascades of key PRR families, including toll-like receptors (TLRs), C-type lectin receptors (CLRs), nucleotide-binding oligomerization domain-like receptors (NLRs), AIM2-like receptors (ALRs), and others. It explores the dual roles of PRRs in immune defense and regulation, particularly through inhibitory PRRs (iPRRs), which prevent immune overactivation. The review also investigates the ligand recognition mechanisms and signaling pathways, highlighting the involvement of PRRs in disease progression and immune modulation. Notable signaling pathways, including NF-κB, MAPK, cGAS-STING, and MYD88-mediated and non-MYD88-mediated cascades, are discussed in the context of immune responses. Mechanisms that fine-tune PRR-mediated responses include transcriptional and fpost-transcriptional regulation, protein degradation, subcellular localization, and the recruitment of amplifiers and inhibitors, along with metabolic and microbial factors. These regulatory strategies ensure immune signaling remains adaptable and precise, preventing excessive inflammation. The review also explores the therapeutic potential of targeting PRRs in treating infectious, inflammatory, autoimmune, and malignant diseases, underscoring their importance in advancing immunological research and precision medicine.</p>","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"149 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144603214","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":"Irinotecan alleviates chemoresistance to anthracyclines through the inhibition of AARS1-mediated BLM lactylation and homologous recombination repair","authors":"Xinyuan Li, Chunlin Zhang, Yuhua Mei, Wenlong Zhong, Wei Fan, Li Liu, Zhenwei Feng, Xuesong Bai, Chuan Liu, Mingzhao Xiao, Weiyang He, Tianxin Lin, Xin Gou","doi":"10.1038/s41392-025-02302-y","DOIUrl":"https://doi.org/10.1038/s41392-025-02302-y","url":null,"abstract":"<p>Chemoresistance remains the major barrier to cancer treatment. Metabolic and epigenetic reprogramming are involved in this process; however, the precise roles and mechanisms are largely unknown. Here, we report that lactate-induced lactylation promotes chemoresistance to anthracyclines by regulating homologous recombination (HR) repair. Using the global lactylome, we revealed the landscape of differentially lactylated sites and proteins in cancer cells isolated from resistant and nonresistant tumors. Specifically, BLM, a crucial helicase in the HR repair process, is highly lactylated at Lys24 by AARS1 in response to chemotherapy. Mechanistically, hyperlactylation of BLM improves its stability by inhibiting MIB1-mediated ubiquitination and increasing its interaction with DNA repair factors, promoting DNA end resection and HR repair. Delactylation of BLM via the Lys24 mutation impairs HR repair and increases anthracycline chemosensitivity. Irinotecan shows synergistic effects and safety for alleviating anthracycline resistance by targeting BLM lactylation and suppressing HR repair in pancancer PDX models. A single-arm, phase I study (identifier NCT06766266) initiated by us suggested that the combination of irinotecan liposomes plus EPI is a feasible and safe treatment strategy for patients with anthracycline-resistant bladder cancer who experience recurrence. These findings exemplify how glycolytic reprogramming regulates HR repair through promoting protein lactylation and highlight the promising therapeutic potential of irinotecan for reversing anthracycline chemoresistance by suppressing BLM lactylation.</p>","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"697 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144594118","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":"Long-term consequences of cancer therapy: cognitive impairment following CAR T cell therapy","authors":"Kathrin Gabriel, Sebastian Kobold","doi":"10.1038/s41392-025-02324-6","DOIUrl":"https://doi.org/10.1038/s41392-025-02324-6","url":null,"abstract":"<p>A recent publication by Geraghty et al. in <i>Cell</i> investigates how chimeric antigen receptor (CAR) T cell therapy can induce cognitive impairment in murine models of both central nervous system (CNS)- and non-CNS-based tumors.¹ The authors identified persistent neuroinflammation as a key mechanism underlying these cognitive deficits and successfully explored novel therapeutic strategies, including microglial depletion and CCR3 blockade (Fig. 1).¹</p><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 1</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1038%2Fs41392-025-02324-6/MediaObjects/41392_2025_2324_Fig1_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 1\" aria-describedby=\"Fig1\" height=\"324\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1038%2Fs41392-025-02324-6/MediaObjects/41392_2025_2324_Fig1_HTML.png\" width=\"685\"/></picture><p>Temporal overview of onset and duration of side effects following administration of CAR T cell therapy. Compared to more acute toxicities such as CRS and ICANS, cognitive impairment can also be seen after months and years following CAR T cell administration. Underlying mechanisms are characterized by distinct neurobiological alterations such as elevated cerebrospinal fluid (CSF) cytokine and chemokine levels, reduced subcortical oligodendrocyte numbers, and microglial activation. Figure created in BioRender. G., K. (2025)</p><span>Full size image</span><svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></figure>","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"192 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144594121","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":"Targeting CD155 in lung adenocarcinoma: A5 nanobody-based therapeutics for precision treatment and enhanced drug delivery","authors":"Kyunghee Noh, Soyeon Yi, Hyeran Kim, Jieun Lee, Suhyeon Kim, Wonbeak Yoo, Eunkyeong Jung, Jinsol Choi, Hwangseo Park, Seungha Hwang, Jin Young Kang, Kwang-Hyun Park, Heewon Park, Yong-kyu Lee, Eun-Kyung Lim, Taejoon Kang, Juyeon Jung","doi":"10.1038/s41392-025-02301-z","DOIUrl":"https://doi.org/10.1038/s41392-025-02301-z","url":null,"abstract":"<p>This study presents a novel approach targeting CD155, an overexpressed protein in lung adenocarcinoma (LUAD), using nanobodies with exceptional precision and efficacy. The significant upregulation of CD155 in LUAD, associated with poor patient outcomes, highlights its potential as a therapeutic target. An anti-CD155 nanobody (A5 Nb) is developed that binds to CD155-positive lung cancer cells with high affinity (A5 Nb <i>K</i>_d = 0.23 nM). The complementarity-determining region of A5 Nb forms hydrophobic interactions and hydrogen bonds with CD155, promoting selective binding and stabilization of A5 Nb-CD155 complex. This interaction inhibits focal adhesion signaling by downregulating paxillin (PXN), leading to a &gt;50% reduction in cell migration. Additionally, A5 Nb conjugated to liposomes loaded with doxorubicin (A5-LNP-DOX) demonstrates a 2- to 3-fold increase in uptake and cytotoxicity in CD155-positive A549 cells, suggesting its potential as a targeted drug delivery system. Therapeutic efficacy was further validated in both lung orthotopic mouse models and lung cancer organoid xenografts, where A5-LNP-DOX exhibited robust antitumor effects and selective targeting. The CD155-PXN axis emerges as a clinically relevant target, correlating with poor outcomes in patients with lung cancer. This study highlights the therapeutic potential of A5 nanobodies in targeting CD155-overexpressing lung cancer cells and offers insights for future developments in lung cancer therapeutics.</p>","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"34 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144594120","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":"Glioblastoma at the crossroads: current understanding and future therapeutic horizons","authors":"Shilpi Singh, Devanjan Dey, Debashis Barik, Iteeshree Mohapatra, Stefan Kim, Mayur Sharma, Sujata Prasad, Peize Wang, Amar Singh, Gatikrushna Singh","doi":"10.1038/s41392-025-02299-4","DOIUrl":"https://doi.org/10.1038/s41392-025-02299-4","url":null,"abstract":"<p>Glioblastoma (GBM) remains the most aggressive and lethal brain tumor in adults and poses significant challenges to patient survival. This review provides a comprehensive exploration of the molecular and genetic landscape of GBM, focusing on key oncogenic drivers, such as epidermal growth factor receptor (EGFR), platelet-derived growth factor receptor (PDGFR), and the PI3K/AKT/mTOR pathway, which are critical for tumorigenesis and progression. We delve into the role of epigenetic alterations, including DNA methylation and histone modifications, in driving therapy resistance and tumor evolution. The tumor microenvironment is known for its pivotal role in immune evasion, with tumor-associated macrophages, myeloid-derived suppressor cells, and regulatory T cells creating an immunosuppressive niche that sustains GBM growth. Emerging therapies, such as immunotherapies, oncolytic viral therapies, extracellular vesicle-based approaches, and non-coding RNA interventions, are highlighted as promising avenues to disrupt GBM pathogenesis. Advances in precision medicine and innovative technologies, including electric field therapy and locoregional treatments, are discussed for their potential to overcome the blood‒brain barrier and treatment resistance. Additionally, this review underscores the importance of metabolic reprogramming, particularly hypoxia-driven adaptations and altered lipid metabolism, in fueling GBM progression and influencing the therapeutic response. The role of glioma stem cells in tumor recurrence and resistance is also emphasized, highlighting the need for targeted therapeutic approaches. By integrating molecular targeting, immune energetics, and technological advancements, this review outlines a multidisciplinary framework for improving GBM treatment outcomes. Ultimately, the convergence of genetic, metabolic, and immune-based strategies offers transformative potential in GBM management, paving the way for increased patient survival and quality of life.</p>","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"109 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144586535","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":"A novel peptide 66CTG stabilizes Myc proto-oncogene protein to promote triple-negative breast cancer growth","authors":"Huichun Liang, Fubing Li, Huan Fang, Wenlong Ren, Zhongmei Zhou, Jiecheng Wang, Jialing Liu, Yongjia Tang, Xue Liu, Yingying Wu, Jing Peng, Chuanyu Yang, Jiayi Chen, Yuting Fei, Yujie Shi, Dewei Jiang, Nu Zhang, Ceshi Chen","doi":"10.1038/s41392-025-02298-5","DOIUrl":"https://doi.org/10.1038/s41392-025-02298-5","url":null,"abstract":"<p>Triple-negative breast cancer (TNBC) is the most malignant subtype of breast cancer that lacks reliable targets for diagnosis and therapy. Non-coding RNA (ncRNA)-encoded products hold promise for addressing this unmet need. By analyzing the reported ribosomal RNA sequencing data, combined with the TCGA, ORFfinder, SmProt databases, we identified CDKN2B-AS1, a TNBC-upregulated lncRNA encoding a 66-amino-acid peptide via CUG-initiated translation. CRISPR-Cas9 gene editing and mass spectrometry confirmed endogenous expression of this peptide, designated 66CTG, in TNBC cells. Functionally independently of its host RNA, 66CTG promoted the proliferation of TNBC cells and the tumor growth of TNBC xenograft by stabilizing c-Myc protein and enhancing Cyclin D1 transcription. Immunohistochemistry of 89 clinical TNBC paraffin samples revealed positive correlations among 66CTG, c-Myc, and Cyclin D1 expression levels. Mechanistically, co-immunoprecipitation and ubiquitination assays revealed that 66CTG stabilized c-Myc by competitively interacting with FBW7α, an E3 ligase responsible for recognizing 66CTG CPD^S56/S60 motif which phosphorylated by GSK-3β during the late G1 phase. In conclusion, our findings suggest 66CTG has potential to be developed as a target for TNBC diagnosis and therapy. Furthermore, it unveils a regulatory axis wherein 66CTG stabilizes c-Myc by interacting with FBW7α, offering a new mechanistic explanation for c-Myc overexpression in TNBC. Patients co-overexpressing 66CTG, c-Myc, and Cyclin D1 may benefit from therapies targeting this axis.</p>","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"33 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144586536","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":"Transferrin receptor 1 nuclear translocation facilitates tumor progression via p53-mediated chromatin interactions and genome-wide alterations","authors":"Yaxin Hou, Guoheng Tang, Qizhi Wang, Meng Zhou, Ran Xu, Xuehui Chen, Guizhi Shi, Zhuoran Wang, Xiyun Yan, Jie Zhuang, Kelong Fan","doi":"10.1038/s41392-025-02297-6","DOIUrl":"https://doi.org/10.1038/s41392-025-02297-6","url":null,"abstract":"<p>Transferrin receptor 1 (TfR1), a widely expressed type II transmembrane glycoprotein located on the plasma membrane, is well known for its established role in cellular iron uptake. Nevertheless, emerging evidence implies that TfR1 exhibits previously unrecognized noncanonical functions. Herein, we demonstrated the nuclear translocation of TfR1 and revealed the interaction between TfR1 and p53 within the nucleus. Through comprehensive analyses at the proteomic, genomic, and transcriptomic levels, we demonstrated that this interaction significantly influences the transcriptional activity of p53 on its downstream target genes, which are highly enriched in DNA damage repair functions. Specifically, our investigation revealed the indispensable role of nuclear TfR1 in the regulation of the nucleotide excision repair (NER) pathway, exemplified by the transcriptional regulation of <i>XPC</i>. Notably, both in vitro and in vivo results revealed a positive regulatory role of TfR1 in the NER pathway. Subsequent phenomic analysis of clinical colorectal tumor samples confirmed a positive correlation between nuclear TfR1 levels and tumor malignancy, aggressive features, and metastasis. Collectively, our findings highlight the non-classical function of TfR1, emphasizing its importance in the regulation of gene expression, as well as tumor progression.</p>","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"29 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144578391","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}