Cell Biology and Toxicology最新文献

{"title":"TCF12-mediated transcriptional activation of CCDC34 is involved in the positive feedback of tumor-associated macrophages and EMT to promote LUSC.","authors":"Jieli Yu, Qinyuan Zhan","doi":"10.1007/s10565-026-10200-4","DOIUrl":"10.1007/s10565-026-10200-4","url":null,"abstract":"<p><p>The positive feedback loop between epithelial-mesenchymal transition (EMT) and M2-like tumor-associated macrophages (TAM-M2) contributes to tumor growth and metastasis. This research aims to investigate the regulatory mechanism of CCDC34 in the maintenance of this loop in lung squamous cell carcinoma (LUSC). Lentiviral vectors were used to knock down CCDC34, and the impact of CCDC34 knockdown on metastasis-like behaviors of LUSC cells was analyzed. LUSC cell-conditioned medium was used to analyze the influence of CCDC34 knockdown in LUSC on the M2 polarization of TAM and to verify the positive feedback loop of EMT and TAM-M2 polarization. CCDC34 was upregulated in LUSC and was related to poor patient prognosis. Knockdown of CCDC34 inhibited EMT in LUSC, decreased M2 polarization of TAM, impaired the positive feedback loop between EMT and TAM-M2 polarization, and suppressed metastasis of mouse LLC cells. TCF12 bound to the CCDC34 promoter to induce its transcription. Overexpression of CCDC34 overturned the blockade of EMT and TAM-M2 polarization by knockdown of TCF12 and promoted metastasis. Consequently, this study elucidates the essential roles of CCDC34 in the positive feedback loop between EMT and TAM-M2 in LUSC, thereby substantiating its potential as a prognostic marker.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13279285/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNAJB4/HLJ1 protects against acetaminophen-induced liver injury by attenuating ER stress via HSP70.","authors":"Chih-Yun Lu, Tsung-Hsuan Hsieh, Min-Hui Chien, Wei-Lun Hsu, Wei-Jia Luo, Jung-Hsuan Chang, Chia-I Lee, Yi-Chun Chen, Cheng-Hao Fang, Ching-Hua Kuo, Sung-Liang Yu, Kang-Yi Su","doi":"10.1007/s10565-026-10198-9","DOIUrl":"10.1007/s10565-026-10198-9","url":null,"abstract":"<p><p>Drug-induced liver injury (DILI) remains a leading cause of acute liver failure; however, current clinical strategies lack reliable biomarkers, predictors of susceptibility, and effective therapeutic interventions. Among these etiologies, acetaminophen (APAP) overdose is the most common cause of DILI worldwide. Heat shock proteins (HSPs), particularly members of the HSP40 family, are central regulators of cellular stress responses, yet the specific role of DNAJB4/HLJ1 in APAP-induced hepatotoxicity remains poorly defined. To address this gap, we employed DNAJB4/HLJ1-deficient mice (Dnajb4^-/-) to investigate the function of DNAJB4/HLJ1 in APAP-induced liver injury. Following APAP administration (> 400 mg/kg), Dnajb4^-/-exhibited exacerbated hepatic necrosis, elevated liver enzymes, and enhanced c-jun/JNK activation compared with Dnajb4^+/+ controls. Metabolic profiling revealed altered APAP metabolism, with reduced detoxification products and excessive oxidative metabolites, and pronounced glutathione (GSH) depletion. Transcriptomic analysis implicated DNAJB4/HLJ1 in metabolism, protein folding, and endoplasmic reticulum (ER) stress via interaction with HSP70. Consistently, ATF6, XBP1, and CHOP expression confirmed aggravated ER stress in Dnajb4^-/- livers. AlphaFold-Multimer modeling and co-immunoprecipitation validated physical interaction between DNAJB4/HLJ1 and HSP70. Restoration of DNAJB4/HLJ1 expression attenuated ER stress, c-jun/JNK activation, and liver injury, while pharmacological inhibition of ER stress confirmed its mechanistic involvement. Collectively, these findings identify DNAJB4/HLJ1 as a previously unrecognized regulator of stress signaling in APAP-induced hepatotoxicity. By modulating ER stress within the integrated cellular stress network, DNAJB4/HLJ1 limits injury progression and promotes hepatocellular resilience, highlighting its potential as a novel therapeutic target for preventing or mitigating DILI.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13279685/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: BMSC‑derived extracellular vesicles affect gluconeogenesis and lipogenesis by releasing 5'‑tRF‑GlyCCC to improve MAFLD insulin sensitivity.","authors":"Chenyun Yang, Huiling Chen, Xiaojing Huang, Yanyan Li, Song Wen, Ligang Zhou, Xinlu Yuan","doi":"10.1007/s10565-026-10187-y","DOIUrl":"10.1007/s10565-026-10187-y","url":null,"abstract":"","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"42 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13106268/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomal miR-145-5p from BMSCs alleviates AKI-induced renal fibrosis via KLHL12/KHSRP-mediated m6A-dependent repression of FLI-1.","authors":"Fanzhou Zeng, Wei Gou, Xuezi Fu, Lingling Ding, Qing Shao, Changhao Zhu, Yuting Liu, Jin Cheng, Bo Yang, Nanmei Liu","doi":"10.1007/s10565-026-10191-2","DOIUrl":"10.1007/s10565-026-10191-2","url":null,"abstract":"<p><p>Pericyte to myofibroblast transformation is a key driver of renal fibrosis following acute kidney injury (AKI). Exosomes, miRNAs, and bone mesenchymal stem cells (BMSCs) are important in alleviating AKI renal fibrosis. We proposed to explore the role of engineering exosomes rich in miR-145-5p and correlated with KLHL12/KHSRP in AKI-induced pericytes-mediated fibrosis in the present study. Rat perirenal cells were isolated and cultured. Engineering exosomes rich in miR-145-5p derived from BMSCs were obtained through cell transfection technology. AKI rat model and Hypoxia/Reoxygenation (HR) induced perirenal cells injury model were established. Dual luciferase reporter gene, MeRIP, and Co-immunoprecipitation were performed to validate miR-145-5p targeting KLHL12 and its downstream molecules including KHSRP and FLI-1. Renal function, apoptosis and pyroptosis, fibrosis-related proteins were detected through biochemistry, immunohistochemistry, immunofluorescence, and transmission electron microscopy to explore the functional role of the miR-145-5p/ KLHL12/KHSRP/FLI-1 axis in cellular and animal models. According to our findings, pericyte-myoblast transformation contributed to AKI-induced fibrosis in vivo and HR-induced fibrosis along with apoptosis and pyroptosis in vitro. MiR-145-5p down-regulated KLHL12 expression by targeting its 3'UTR to improve perirenal cells-mediated fibrosis. KLHL12 might downregulate KHSRP to increase FLI-1 expression by promoting FLI-1 mRNA stability in AKI-induced fibrosis mediated by perirenal cells. These findings indicate that miR-145-5p enriched in BMSC derived engineered exosomes may suppress KLHL12 expression to up-regulate KHSRP and then down-regulate FLI-1 by m6A to attenuate perirenal cells-mediated fibrosis.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13230268/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147728163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: CD44‑targeted therapy using mP6/Rg3 micelles inhibits oral cancer stem cell proliferation and migration.","authors":"Sijia Cai, Yuwen Chen, Changyu Chen, Ming Liu","doi":"10.1007/s10565-026-10185-0","DOIUrl":"10.1007/s10565-026-10185-0","url":null,"abstract":"","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"42 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13095910/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147728255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell transcriptome profiling reveals the heterogeneity of ossification of the posterior longitudinal ligament (OPLL) and its immune microenvironment.","authors":"Zhongyuan He, Jiaxiang Zhou, Fuan Wang, Peng Guo, Jianfeng Li, Zhengya Zhu, Tao Tang, Nguyen Tran Canh Tung, Yoshiharu Kawaguchi, Shaoyu Liu, ManMan Gao, Xizhe Liu, Zhiyu Zhou","doi":"10.1007/s10565-026-10193-0","DOIUrl":"10.1007/s10565-026-10193-0","url":null,"abstract":"<p><strong>Background: </strong>Ossification of the posterior longitudinal ligament (OPLL) is a heterotopic ossification process of the posterior longitudinal ligament (PLL) that can compress the spinal cord and nerve roots, yet its cellular heterogeneity and pathogenesis remain unclear.</p><p><strong>Methods: </strong>We performed single-cell RNA sequencing (scRNA-seq) with integrative computational analyses and histological validation on 4,683 cells from surgically resected cervical OPLL lesions obtained from human patients.</p><p><strong>Results: </strong>We identified 15 major cell subsets, including chondrocyte-lineage populations-progenitor/proliferative fibrocartilage chondrocytes (ProFCs), pre-hypertrophic chondrocytes (preHTCs), and hypertrophic chondrocytes (HTCs)-as well as osteoblasts, endothelial cells, and diverse immune cells. Pseudotime analysis suggested an inferred trajectory from cartilage progenitor-like cells through inflammatory/reactive and hypertrophic states toward osteogenic programs, with progressive activation of ossification, extracellular-matrix, and inflammation-related pathways. Cell-cell communication analyses showed coordinated immune-stromal crosstalk, with FGF signaling enriched in earlier pseudotime states and SPP1-CD44 signaling enriched in later states. SPP1 signals originated predominantly from HTCs, whereas macrophages were prominently involved in the broader inflammatory niche and immune-stromal communication within OPLL lesions. Consistently, SPP1/CD44-positive cells were enriched in OPLL tissues and further increased by IL-1β stimulation in vitro and in an Enpp1-driven OPLL mouse model.</p><p><strong>Conclusions: </strong>This exploratory single-cell atlas suggests that an inflammatory niche may couple chondrocyte hypertrophy with osteogenic activation and highlights candidate immune-stromal pathways for future biomarker and therapeutic exploration in OPLL.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13219239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147716212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Titanium dioxide nanoparticles in oncology: synthesis, application, and challenges.","authors":"Parth Agarwal, Rachana Raman, Rushil Dalal, Harshil Jain, Ajaatshatru Sisodia, Prasoon Agarwal, Praveen Kumar","doi":"10.1007/s10565-026-10190-3","DOIUrl":"10.1007/s10565-026-10190-3","url":null,"abstract":"<p><p>Nanoparticles (NPs) are defined as particles that have a diameter less than 100 nm. Titanium dioxide (TiO₂) NPs (TiO₂ NPs) have gained significant attention in recent years as a possible therapeutic agent due to their unique physiochemical properties. They include tunability of the NPs, effective dopant compatibility, biocompatibility and catalytic properties. The shape and size of the NPs also play an important role in TiO₂ NPs for its efficiency in drug encapsulation, circulation time, efficacy and aggregation. The most effective size for TiO₂ NPs ranges from 20-150 nm, with the preferred shape being spherical. TiO₂ NPs, although largely ineffective as the sole therapeutic agent, have shown the ability to reduce tumorigenesis and augment the efficacy of cancer therapy in a range of cancers and treatments, such as photodynamic therapy (PDT), sonodynamic therapy (SDT), photothermal therapy (PTT), immunotherapy, and chemotherapy. However, TiO₂ NPs have been associated with cytotoxic and genotoxic effects in several settings, which are discussed in this review. Regulatory barriers hinder its applicability, and are directly related to long-term toxicity due to prolonged exposure. These obstacles have hindered translation of these NP-based technologies in clinical settings. This highlights the need to conduct further research to address possible concerns regarding toxicity and safety even after long-term exposure. In this review, we discuss the mechanism of TiO₂ NPs as a DDA, its applications in cancer therapy, potential risks, as well as strategies to minimize its associated risks.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13216158/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147716196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Revealing an enhanced cytotoxic immune microenvironment at the human maternal-fetal interface in preeclampsia.","authors":"Yueli Mu, Dong Liu, Zhuoxu He, Julin Wang, Wenjie Zhou, Hongqin Chen, Shengping Zhou, Ting Feng, Rong Zhou, Hong Li","doi":"10.1007/s10565-026-10170-7","DOIUrl":"10.1007/s10565-026-10170-7","url":null,"abstract":"<p><p>Preeclampsia is a multifactorial pregnancy complication characterized by hypertension and immune dysregulation, which can lead to adverse maternal and fetal outcomes. Decidual immune cells are critical for pregnancy homeostasis, yet their functional abnormalities and mechanisms in preeclampsia remain poorly understood. Herein, we sorted decidua immune cells from preeclampsia patients for single-cell RNA sequencing to characterize cellular composition and functional heterogeneity. We delineated the immune cell landscape of the decidua in preeclampsia. A hallmark of decidual immune microenvironment in preeclampsia was the marked augmentation of cytotoxic activity. Both NK and T cells exhibited enhanced cytotoxic activity, characterized by the significant upregulation of cytotoxicity-associated genes. NK cells exhibited a differentiation predisposition toward a unique tissue-resident ITGAE⁺CD160⁺ subset with heightened cytotoxic and chemokine gene expression. Cell-cell communication analysis further revealed strengthened interactions between NK cells and macrophages, with macrophage-derived SPP1 signals potentially contributing to the amplification of local cytotoxic responses. Collectively, this study provides a comprehensive single-cell analysis of cytotoxic immune changes at the maternal-fetal interface in preeclampsia, revealing enhanced cytotoxicity that may represent a key pathological mechanism. These insights may inform the development of diagnosis and therapeutic strategies targeting cytotoxic immune dysregulation in PE.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13315417/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell RNA sequencing reveals HMGA2 involvement in neoplastic aggressiveness and endothelial cell senescence in chondrosarcoma.","authors":"Shenglin Wang, Shuting Lu, Xinwen Wang, Hongxiang Wei, Huarong Zhang, Weixin Zhou, Jie Lin, Xueyi Huang, Fude Liang, Zhaoyang Wu, Jianhua Lin, Xiaopei Shen, Lu Ao","doi":"10.1007/s10565-026-10188-x","DOIUrl":"10.1007/s10565-026-10188-x","url":null,"abstract":"<p><p>Chondrosarcoma (CHS) is a malignant bone tumor resistant to adjuvant treatment, with high-grade patients suffering an unfavorable prognosis. Therefore, a deeper insight into the tumor microenvironment is essential for developing effective treatments for advanced CHS. To decipher the cellular heterogeneity between CHS with differential malignancy and benign cartilage tumors, we performed single-cell RNA sequencing (scRNA-seq) on clinical specimens of high- and low-grade CHS, endochondroma and paratumoral tissues. The findings of transcriptional characteristics were validated by the bioinformatics analyses of public bulk datasets. The role of markers of interest was further explored by histological staining, in vitro and in vivo experiments. The results demonstrated that neoplastic cells and stromal cells predominated in the CHS tumor microenvironment. High-grade CHS presented aggravated proliferation and angiogenesis characteristics in neoplastic cells. The in silico analysis and functional experiments identified HMGA2 as a regulator of these malignant phenotypes and an independent predictor of poor outcome. Tumor-associated endothelial cells (TA-ECs) in CHS demonstrated senescent yet aggressive phenotypes underpinned by HBEGF. Moreover, HCHS exhibited more prevalent cellular communications between neoplastic cells and TA-ECs mediated by SPP1 and EGF pathways, with SPP1 and HBEGF both predicting unfavorable prognosis. Mechanistically, HMGA2 induced neoplastic secretion of SPP1, which provoked endothelial senescence and HBEGF release. Our findings implicate malignant characteristics in neoplastic cells and endothelial senescence associated with the histological grade of CHS and underscore the potential value of HMGA2 and SPP1 as actionable therapeutic targetes for advanced patients.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13186804/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147662237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pre-treatment with baicalein alleviates the diquat-induced microglial pyroptosis through gut microbiota-derived indole-3-propionic acid and DDX3X/G3BP1 pathway.","authors":"Ting Li, Mengxiao Feng, Ping Wang, Miao Jiang, Jaiyu Cui, Mengxia Jin, Congying Song, Liying Lin, Yuan-Qiang Lu","doi":"10.1007/s10565-026-10189-w","DOIUrl":"10.1007/s10565-026-10189-w","url":null,"abstract":"<p><p>Baicalein, a naturally occurring flavonoid with well-documented anti-inflammatory and neuroprotective effects, has shown therapeutic promise in multiple models of neurological disorders. However, whether baicalein can counteract diquat-induced neurotoxicity remains uncertain. This study reveals that baicalein alleviates diquat-induced neuroinflammation and microglial pyroptosis in mice in a gut microbiota (GM)-dependent manner. In the in vivo experiments, multi-omics analyses demonstrated that baicalein elevates the GM-derived metabolite indole-3-propionic acid (IPA), which was sufficient to suppress pyroptosis. In parallel, IPA was identified as a critical mediator of baicalein's neuroprotective effects, as exogenous IPA administration recapitulated baicalein's protection, and baicalein treatment significantly elevated IPA levels. Mechanistically, through inhibiting the DEAD-box helicase 3 X-linked / GTPase-activating protein (SH3 domain) binding protein 1 pathway by in vitro experiments. Our study demonstrated that baicalein mitigates diquat-induced neuroinflammation, underscoring the therapeutic potential of targeting the GM to counteract herbicide-related neurotoxicity.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13186918/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147643997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}