{"title":"Retinol Binding Protein 4 reactivates latent HIV-1 by triggering canonical NF-κB, JAK/STAT5 and JNK signalling.","authors":"Chiara Pastorio,Khumoekae Richard,Shariq Usmani,Ann-Kathrin Kissmann,Grigory Bolotnikov,Guillermo Gosálbez,Manuel Hayn,Lennart Koepke,Alina Sauertnik,Andrea Preising,Nico Preising,Ludger Ständker,Matthew Fair,Jessicamarie Morris,Emmanouil Papasavvas,Qin Liu,Honghong Sun,Armando Rodríguez,Karam Mounzer,Sebastian Wiese,Pablo Tebas,Yangzhu Du,Gregory M Laird,Markus Jaritz,Frank Rosenau,Moritz M Gaidt,Konstantin M J Sparrer,Luis J Montaner,Frank Kirchhoff","doi":"10.1038/s41392-025-02424-3","DOIUrl":"https://doi.org/10.1038/s41392-025-02424-3","url":null,"abstract":"Reactivation of the latent viral reservoirs is crucial for a cure of HIV/AIDS. However, current latency reversing agents are inefficient, and the endogenous factors that have the potential to reactivate HIV in vivo remain poorly understood. To identify natural activators of latent HIV-1, we screened a comprehensive peptide/protein library derived from human hemofiltrate, representing the entire blood peptidome, using J-Lat cell lines harboring transcriptionally silent HIV-1 GFP reporter viruses. Fractions potently reactivating HIV-1 from latency contained human Retinol Binding Protein 4 (RBP4), the carrier of retinol (Vitamin A). We found that retinol-bound holo-RBP4 but not retinol-free apo-RBP4 strongly reactivates HIV-1 in a variety of latently infected T cell lines. Functional analyses indicate that this reactivation involves activation of the canonical NF-κB pathway and is strengthened by JAK/STAT5 and JNK signalling but does not require retinoic acid production. High levels of RBP4 were detected in plasma from both healthy individuals and people living with HIV-1. Physiological concentrations of RBP4 induced significant viral reactivation in latently infected cells from individuals on long-term antiretroviral therapy with undetectable viral loads. As a potent natural HIV-1 latency-reversing agent, RBP4 offers a novel approach to activating the latent reservoirs and bringing us closer to a cure.","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"214 1","pages":"326"},"PeriodicalIF":39.3,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145209052","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}
Seungmo Kim,Yongjoong Kim,Tae-Sung Kim,Jae-Hyeok Kang,In-Yeong Yun,Eung-Suk Lee,Eun Ji Lee,Rae-Kwon Kim,Joo Mi Yi,Hye Sook Choi,Jin Woo Song,Young Woo Jin,Min-Jung Kim,Su-Jae Lee
{"title":"Colony-stimulating factor 3 as a key mediator in the progression of idiopathic pulmonary fibrosis: a novel therapeutic target.","authors":"Seungmo Kim,Yongjoong Kim,Tae-Sung Kim,Jae-Hyeok Kang,In-Yeong Yun,Eung-Suk Lee,Eun Ji Lee,Rae-Kwon Kim,Joo Mi Yi,Hye Sook Choi,Jin Woo Song,Young Woo Jin,Min-Jung Kim,Su-Jae Lee","doi":"10.1038/s41392-025-02421-6","DOIUrl":"https://doi.org/10.1038/s41392-025-02421-6","url":null,"abstract":"Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease characterized by excessive ECM deposition and myofibroblast accumulation driven by cytokine dysregulation. This study identified granulocyte colony-stimulating factor 3 (CSF3) as a key mediator of IPF progression. Elevated CSF3 expression was observed in the lung tissues of IPF patients. Recombinant CSF3 promoted myofibrogenesis in lung fibroblasts, whereas CSF3-deficient mice were protected from bleomycin-induced pulmonary fibrosis. Treatment with novel CSF3-neutralizing antibodies significantly restored fibrosis in IPF mice by suppressing myofibroblast differentiation and reducing ECM deposition. Here, we demonstrated a reciprocal regulatory relationship between CSF3 and TGF-β that amplifies pro-fibrotic signaling. Our mechanistic studies revealed that CSF3 acts as an upstream regulator of TGF-β, forming a positive feedback loop that significantly accelerates the fibrotic process. Knockout or neutralization of CSF3 suppressed fibrosis by reducing TGF-β levels, whereas treatment with recombinant CSF3 promoted fibrosis with increased TGF-β expression. Notably, while CSF3 inhibition reduced TGF-β expression levels, it did not decrease them below normal levels. This finding suggests that inhibiting CSF3 could simultaneously reduce fibrosis by suppressing excessive TGF-β expression while also minimizing side effects by maintaining TGF-β homeostasis. Taken together, these results provide strong evidence that CSF3 is a critical driver of IPF pathogenesis and that targeting CSF3 may provide a therapeutic strategy by modulating TGF-β signaling and restoring the ECM and cellular homeostasis.","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"114 1","pages":"322"},"PeriodicalIF":39.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145203565","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":"Multiple sclerosis: molecular pathogenesis and therapeutic intervention.","authors":"Imane Boutitah-Benyaich,Herena Eixarch,Javier Villacieros-Álvarez,Arnau Hervera,Álvaro Cobo-Calvo,Xavier Montalban,Carmen Espejo","doi":"10.1038/s41392-025-02415-4","DOIUrl":"https://doi.org/10.1038/s41392-025-02415-4","url":null,"abstract":"Multiple sclerosis is a chronic immune-mediated disorder of the central nervous system characterized by demyelination, axonal loss, and neuroinflammation, culminating in progressive neurological disability. Despite significant advances in understanding its immunopathogenesis, current immunotherapies remain limited in their ability to halt disease progression, making multiple sclerosis incurable and highlighting the critical need for novel therapeutic strategies. Antigen-specific immunotherapy represents a groundbreaking approach that aims to restore immune tolerance to myelin-derived antigens while preserving the protective functions of the immune system. Unlike broad immunosuppressive strategies, antigen-specific immunotherapy offers the potential for highly targeted modulation of pathogenic immune responses, reducing off-target effects and enhancing safety profiles. Over the last two decades, preclinical studies and clinical trials have explored diverse antigen-specific immunotherapy modalities, ranging from peptide-based vaccines to nanoparticle platforms, each aimed at achieving durable tolerance in multiple sclerosis. This review provides a comprehensive overview of multiple sclerosis, covering its etiology, clinical features, pathogenesis, pathology, and current therapeutic approaches. Thus, it delves into the current state of antigen-specific immunotherapy research, critically examining its successes and limitations while addressing the translational challenges that must be overcome to realize its therapeutic potential. By integrating insights from immunology, biotechnology, and translational medicine, we propose directions for advancing antigen-specific approaches in the quest for transformative multiple sclerosis therapies.","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"76 1","pages":"324"},"PeriodicalIF":39.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145203562","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":"Sodium nitrate protects against metabolic syndrome by sialin-mediated macrophage rebalance.","authors":"Shaorong Li,Yaning Wang,Zihan Zhang,Haozhe Xu,Songyue Wu,Hua Jin,Xiaotong Han,Ying Liu,Xin Wen,Yi Wu,Zhongtao Zhang,Lei Hu,Liang Hu,Chunmei Zhang,Jinsong Wang,Renhong Yan,Mo Chen,Guozhi Xiao,Guangyong Sun,Dong Zhang,Songlin Wang","doi":"10.1038/s41392-025-02418-1","DOIUrl":"https://doi.org/10.1038/s41392-025-02418-1","url":null,"abstract":"Metabolic syndrome, characterized by metabolic dysfunction-associated steatotic liver disease (MASLD) and type 2 diabetes mellitus (T2DM), poses a significant threat to patients' health worldwide; however, efficient treatment is currently unavailable. Here, we show that oral administration of sodium nitrate (NaNO3) greatly attenuates the development and advancement of MASLD-like and T2DM-like phenotypes in mice induced by choline-deficient high-fat, western, or methionine/choline-deficient diet. NaNO3 attenuates metabolic turbulence by rebalancing CD206+/CD11C+ polarization (anti-inflammatory/pro-inflammatory) and the function of bone marrow-derived macrophages (MoMFs). Using metabolic disorder animal models and bone marrow-reconstituted mice with mutated gene function in Slc17a5, which encodes sialin, we demonstrate that NaNO3 protects against metabolic disorders through the actions of sialin in MoMFs. NaNO3 can directly regulate MoMFs polarization and function in vitro and in mice, in which nitric oxide production from oral and enteral symbiotic bacteria is essentially abolished. At the molecular level, sialin, via the inhibition of the key transcription factor Rel, inhibits cathepsin L (CtsL) expression and thereby activates the Nrf2 pathway to modulate macrophage homeostasis and ameliorate metabolic abnormalities. Interestingly, the sialin-CtsL-Nrf2 pathway is downregulated in human macrophages from metabolic dysfunction-associated steatohepatitis (MASH) patients. Overall, we demonstrate the prophylactic and therapeutic effects of NaNO3 on metabolic syndrome and reveal a new macrophage rebalancing strategy involving NaNO3 through a novel sialin pathway. Our research indicates that NaNO3 may be a pharmaceutical agent for managing and alleviating metabolic turbulence in humans.","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"7 1","pages":"323"},"PeriodicalIF":39.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145203559","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 long interspersed nuclear element-1 by nucleoside reverse transcriptase inhibitors attenuates vascular calcification.","authors":"Jianshuai Ma,Dayu He,Mingxuan Zhang,Ziting Zhou,Jinkun Cheng,Aoran Huang,Yaxin Lian,Yuncong Shi,Changming Xie,Zhengyan Guan,Zhengzhipeng Zhang,Chen Xie,Tingting Zhang,Hui Huang","doi":"10.1038/s41392-025-02396-4","DOIUrl":"https://doi.org/10.1038/s41392-025-02396-4","url":null,"abstract":"Vascular calcification (VC) is a critical vascular pathological event, contributing to the rise in both the prevalence and fatality of cardiovascular diseases. However, the lack of effective therapeutic strategies for VC is attributed primarily to the incomplete understanding of its underlying molecular mechanisms. In this study, we discovered that long interspersed nuclear element 1 (LINE1) was significantly upregulated in the calcified arteries of both human individuals and mouse models. Mechanistically, silencing LINE1 expression or inhibiting its activity with adding nucleoside reverse transcriptase inhibitors (NRTIs, a class of validated LINE1 inhibitors) effectively prevented the osteogenic reprogramming of vascular smooth muscle cells (VSMCs). Moreover, NRTIs treatment substantially mitigated VC in chronic kidney disease (CKD)-induced and vitamin D3-overloaded VC mouse models. RNA sequencing analysis revealed that LINE1 depletion (via small interfering RNA) or NRTIs intervention downregulated the cGAS-STING signaling pathway and its associated inflammatory genes in VSMCs. Functional validation revealed that stimulation of the cGAS‒STING pathway exacerbated VC, whereas its pharmacological inhibition alleviated VC. Notably, we identified LINE1-derived cDNA as a direct activator of the cGAS‒STING pathway, demonstrating that LINE1 inhibition suppresses VC by blocking cGAS‒STING activation and subsequent inflammatory responses. Clinically, a cross-sectional study involving 1,785 participants revealed that patients receiving NRTIs therapy presented a significantly lower incidence of VC and reduced calcification scores. Multivariate logistic regression analysis further confirmed that NRTIs use is an independent protective factor against VC incidence and progression. Collectively, these findings establish LINE1 as promising therapeutic targets for VC and highlight NRTIs as potential candidates for developing novel strategies against VC.","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"7 1","pages":"321"},"PeriodicalIF":39.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145194636","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}
Claire M Storey,Mohamed Altai,Katharina Lückerath,Wahed Zedan,Henan Zhu,Lara Breuer,Marija Trajkovic-Arsic,Julie Park,Abbie Hasson,Jens Siveke,Diane Abou,Haley Marks,Enna Ulmert,Alexander Ridley,Marcella Safi,Urpo Lamminmäki,Constance Yuen,Susanne Geres,Liqun Mao,Michael Cheng,Sumit K Subudhi,Bilal A Siddiqui,Noah Federman,Johannes Czernin,Ken Herrmann,Laurent Bentolila,Xia Yang,Thomas G Graeber,Robert Damoiseaux,Daniel Thorek,David Ulmert
{"title":"Development of a leucine-rich repeat-containing protein 15-targeted radio-immunotheranostic approach to deplete pro-tumorigenic mechanisms and immunotherapy resistance.","authors":"Claire M Storey,Mohamed Altai,Katharina Lückerath,Wahed Zedan,Henan Zhu,Lara Breuer,Marija Trajkovic-Arsic,Julie Park,Abbie Hasson,Jens Siveke,Diane Abou,Haley Marks,Enna Ulmert,Alexander Ridley,Marcella Safi,Urpo Lamminmäki,Constance Yuen,Susanne Geres,Liqun Mao,Michael Cheng,Sumit K Subudhi,Bilal A Siddiqui,Noah Federman,Johannes Czernin,Ken Herrmann,Laurent Bentolila,Xia Yang,Thomas G Graeber,Robert Damoiseaux,Daniel Thorek,David Ulmert","doi":"10.1038/s41392-025-02410-9","DOIUrl":"https://doi.org/10.1038/s41392-025-02410-9","url":null,"abstract":"Leucine-rich repeat containing 15 (LRRC15) has emerged as an attractive biomarker and target for cancer therapy. Transforming growth factor-β (TGFβ) induces the expression of this plasma membrane protein specifically in aggressive and treatment resistant tumor cells derived from mesenchymal stem cells, with minimal expression observed in non-neoplastic tissues. We have developed a humanized monoclonal antibody, DUNP19, that specifically binds with high affinity to a phylogenetically conserved LRRC15 epitope and is rapidly internalized upon LRRC15 binding. In multiple subcutaneous and orthotopic tumor xenograft mouse models, Lutetium-177 labeled DUNP19 ([177Lu]Lu-DUNP19) enabled non-invasive imaging and molecularly precise radiotherapy to LRRC15-expressing cancer cells and murine cancer-associated fibroblasts, effectively halting tumor progression and prolonging survival with minimal toxicity. Transcriptomic analyses of [177Lu]Lu-DUNP19-treated tumors reveal a loss of pro-tumorigenic mechanisms, including a previously reported TGFβ-induced LRRC15+ signature associated with immunotherapy resistance. In a syngeneic tumor model, administration of [177Lu]Lu-DUNP19 significantly potentiated checkpoint-blockade therapy, yielding durable complete responses. Together, these results demonstrate that radio-theranostic targeting of LRRC15 with DUNP19 is a compelling precision medicine platform for image-guided diagnosis, eradication, and reprogramming of LRRC15+ tumor tissue that drives immuno-resistance and disease aggressiveness in a wide range of currently untreatable malignancies.","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"5 1","pages":"319"},"PeriodicalIF":39.3,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145189453","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":"Consolidative nivolumab versus observation in unresectable stage III non-small cell lung cancer patients following neoadjuvant nivolumab plus chemotherapy and concurrent chemoradiotherapy (CA209-7AL): a randomized clinical trial.","authors":"Bo Qiu,Yuanyuan Zhao,Wenzhuo He,Weijin Zeng,Hongmei Zhang,Weineng Feng,Jun Jia,Daodu Wang,Daquan Wang,Fangjie Liu,Songran Liu,Shaohan Yin,Chuanmiao Xie,Rui Zhou,Yi Hu,Qianwen Liu,Jinyu Guo,Suping Guo,Yingjia Wu,Qiaoting Luo,Jibin Li,Yunpeng Yang,Liangping Xia,Li Zhang,Hui Liu","doi":"10.1038/s41392-025-02408-3","DOIUrl":"https://doi.org/10.1038/s41392-025-02408-3","url":null,"abstract":"CA209-7AL is a randomized, multicenter, phase 2 trial evaluating the efficacy and safety of consolidative nivolumab (NIVO) versus observation following neoadjuvant NIVO plus chemotherapy and concurrent chemoradiotherapy (CCRT) for unresectable stage III NSCLC. Patients received 2 cycles of neoadjuvant chemo-NIVO therapy (docetaxel + cisplatin + NIVO) and CCRT (total dose 54-64 Gy). Post-CCRT, eligible patients were randomized 1:1 to receive consolidative NIVO (360 mg every 3 weeks for up to 12 months) or observation. The primary endpoint was progression-free survival (PFS) from randomization. Between December 3rd, 2019, and August 18th, 2023, 264 patients were enrolled, and 172 were randomized to NIVO consolidation (n = 86) or observation (n = 86). With a median follow-up of 22·8 months, NIVO consolidation resulted in significantly longer PFS than did observation (median not reached vs. 12.2 months [95% CI 10.2-20.8]; stratified hazard ratio 0·49 [95% CI 0.30-0.79], p = 0.003). NIVO consolidation also demonstrated superior PFS compared with a parallel real-world study, where patients received CCRT followed by consolidative immunotherapy (median PFS: 15.7 months [95% CI 11.9-NA]). Grade 3 or 4 toxicities occurred in 9.3% of patients in the consolidation group versus 4·6% in the observation group, with similar rates of pneumonitis (2.3% each) and proximal bronchial tree toxicity (3.5% vs. 2.3%). Treatment-related death occurred in 1 (1.2%) patient in the consolidation group because of pneumonitis. Patients with a high TMB had a longer PFS with consolidation (NR vs. 15.2 months, p = 0.042). Consolidative NIVO following neoadjuvant NIVO plus chemotherapy and CCRT demonstrated effectiveness and tolerability for patients with unresectable stage III NSCLC (ClinicalTrials.gov NCT04085250).","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"66 1","pages":"317"},"PeriodicalIF":39.3,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145182553","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":"Tumor microenvironment delineates differential responders to trastuzumab emtansine in HER2-positive metastatic breast cancer patients previously treated with pyrotinib: an exploratory biomarker analysis of a phase II study (NJMU-BC02).","authors":"Hong Pan,Ji Wang,Yue Sun,Fanfan Li,Chang Sun,Mingduo Liu,Hong Xu,Jing Tao,Xinrui Mao,Cong Wang,Shui Wang,Wei Li,Qiang Ding,Wenbin Zhou","doi":"10.1038/s41392-025-02409-2","DOIUrl":"https://doi.org/10.1038/s41392-025-02409-2","url":null,"abstract":"Trastuzumab emtansine (T-DM1) has been approved for the treatment of HER2-positive breast cancer. However, the efficacy of T-DM1 for patients after failure of pyrotinib and/or trastuzumab plus pertuzumab has not been clear. Additionally, no biomarker has been reported to predict the effect of T-DM1. In this multicenter phase II trial (NCT06125834), 36 participants with HER2-positive metastatic breast cancer were enrolled to receive T-DM1 therapy on a 21-day cycle until progression or unacceptable toxicity. The primary endpoint was the objective response rate (ORR). The secondary endpoints included the disease control rate (DCR), clinical benefit rate (CBR), progression-free survival (PFS), and toxicity. The primary endpoint was an ORR of 47.2% (17/36, 95% CI 30.4-64.5). The treatment exhibited a manageable toxicity profile. The DCR was 66.7% (24/36, 95% CI 49.0-81.4), and the CBR was 50.0% (18/36, 95% CI 32.9-67.1). The median PFS was 6.6 (95% CI 5.2-NA) months. Single-cell RNA sequencing revealed that the low cell cycle activity of cancer cells, activated macrophages and CD8+ T cells was associated with the good efficacy of T-DM1, which was validated in a neoadjuvant cohort. This study suggests that T-DM1 is effective with a measurable safety profile in patients with metastatic HER2-positive breast cancer after failure of pyrotinib and/or trastuzumab plus pertuzumab. Our preliminary findings suggest potential biomarkers that may help predict T-DM1 efficacy, generating hypotheses for novel therapeutic targets that may address T-DM1 resistance.","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"96 1","pages":"318"},"PeriodicalIF":39.3,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145182557","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}
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