Cell Biology and Toxicology最新文献

{"title":"UHRF1 promotes calcium oxalate-induced renal fibrosis by renal lipid deposition via bridging AMPK dephosphorylation.","authors":"Yushi Sun, Bojun Li, Baofeng Song, Yuqi Xia, Zehua Ye, Fangyou Lin, Xiangjun Zhou, Wei Li, Ting Rao, Fan Cheng","doi":"10.1007/s10565-025-09991-9","DOIUrl":"https://doi.org/10.1007/s10565-025-09991-9","url":null,"abstract":"<p><strong>Background: </strong>Nephrolithiasis, a common urinary system disorder, exhibits high morbidity and recurrence rates, correlating with renal dysfunction and the increased risk of chronic kidney disease. Nonetheless, the precise role of disrupted cellular metabolism in renal injury induced by calcium oxalate (CaOx) crystal deposition is unclear. The purpose of this study is to investigate the involvement of the ubiquitin-like protein containing PHD and RING finger structural domain 1 (UHRF1) in CaOx-induced renal fibrosis and its impacts on cellular lipid metabolism.</p><p><strong>Methods: </strong>Various approaches, including snRNA-seq, transcriptome RNA-seq, immunohistochemistry, and western blot analyses, were employed to assess UHRF1 expression in kidneys of nephrolithiasis patients, hyperoxaluric mice, and CaOx-induced renal tubular epithelial cells. Subsequently, knockdown of UHRF1 in mice and cells corroborated its effect of UHRF1 on fibrosis, ectopic lipid deposition (ELD) and fatty acid oxidation (FAO). Rescue experiments using AICAR, ND-630 and Compound-C were performed in UHRF1-knockdown cells to explore the involvement of the AMPK pathway. Then we confirmed the bridging molecule and its regulatory pathway in vitro. Experimental results were finally confirmed using AICAR and chemically modified si-UHRF1 in vivo of hyperoxaluria mice model.</p><p><strong>Results: </strong>Mechanistically, UHRF1 was found to hinder the activation of the AMPK/ACC1 pathway during CaOx-induced renal fibrosis, which was mitigated by employing AICAR, an AMPK agonist. As a nuclear protein, UHRF1 facilitates nuclear translocation of AMPK and act as a molecular link targeting the protein phosphatase PP2A to dephosphorylate AMPK and inhibit its activity.</p><p><strong>Conclusion: </strong>This study revealed that UHRF1 promotes CaOx -induced renal fibrosis by enhancing lipid accumulation and suppressing FAO via inhibiting the AMPK pathway. These findings underscore the feasible therapeutic implications of targeting UHRF1 to prevent renal fibrosis due to stones.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"39"},"PeriodicalIF":5.3,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Esketamine alleviates depressive-like behavior in neuropathic pain mice through the METTL3-GluA1 pathway.","authors":"Xiaoming Ji, Zhimin Huang, Chenming Zhou, Yu Wang, Dongliang Geng, Guoliang Zhang, Yunxiao Kang, Rui Cui, Jinyang Wang, Tianyun Zhang","doi":"10.1007/s10565-024-09975-1","DOIUrl":"10.1007/s10565-024-09975-1","url":null,"abstract":"<p><p>Esketamine, a newly developed antidepressant, is the subject of this research which seeks to explore its impact on depressive symptoms in neuropathic pain mice and the potential molecular mechanisms involved. Through transcriptome sequencing and bioinformatics analysis combined with in vivo studies, it was identified that esketamine markedly boosts the levels of the m6A methyltransferase METTL3 and the AMPA receptor GluA1 subunit. Esketamine activates METTL3, allowing it to bind with GluA1 mRNA, promoting m6A modification, thereby enhancing GluA1 expression at synapses. Through this mechanism, esketamine may reduce depressive-like behavior in neuropathic pain mice, providing new insights into the potential applications of esketamine and novel therapeutic avenues for neuropathic pain and depressive behavior.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"38"},"PeriodicalIF":5.3,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11775062/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058312","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":"Targeting p38γ synergistically enhances sorafenib-induced cytotoxicity in hepatocellular carcinoma.","authors":"Chen Huang, Chenliang Zhang, Jiajin Li, Yichun Duan, Qiulin Tang, Feng Bi","doi":"10.1007/s10565-024-09979-x","DOIUrl":"10.1007/s10565-024-09979-x","url":null,"abstract":"<p><p>Sorafenib (Sora) is a first-line treatment for patients with advanced hepatocellular carcinoma (HCC). It can significantly improve the survival rate of patients with advanced HCC, but it is prone to drug resistance during treatment, so the therapeutic effect is extremely limited. Here, we demonstrate that an elevated expression of protein kinase p38γ in hepatocellular carcinoma cells diminishes the tumor cells' sensitivity to Sora. Pirfenidone (PFD) can augment Sora's inhibitory effect on hepatocellular carcinoma by specifically targeting p38γ. Our study further uncovers that pirfenidone can synergistically boost the anti-hepatocellular carcinoma impact of Sora by impeding the autophagy heightened by p38γ. Taken together, our findings suggest that pirfenidone can work in concert with Sora to intensify its anti-tumor effect on hepatocellular carcinoma, thereby offering a novel therapeutic approach for Sora-mediated tumor treatment.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"35"},"PeriodicalIF":5.3,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11772449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051808","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":"Comparative characterization of organ-specific phase I and II biotransformation enzyme kinetics in salmonid S9 sub-cellular fractions and cell lines.","authors":"Baptiste P M Martin, Marco E Franco, Kristin Schirmer","doi":"10.1007/s10565-025-09992-8","DOIUrl":"10.1007/s10565-025-09992-8","url":null,"abstract":"<p><p>Advancing in vitro systems to address the effects of chemical pollution requires a thorough characterization of their functionalities, such as their repertoire of biotransformation enzymes. Currently, knowledge regarding the presence, activity magnitudes, and inducibility of different biotransformation pathways in vitro is scarce, particularly across organs. We report organ-specific kinetics for phase I and II biotransformation enzymes, under basal and induced conditions, in two in vitro systems using salmonid fish: S9 sub-cellular fractions from brown trout (Salmo trutta) and rainbow trout (Oncorhynchus mykiss) were compared with rainbow trout cell lines. Cyp1a and glutathione S-transferase (Gst) activities were the highest in liver S9 fractions and RTL-W1 liver cells, yet systems derived from the intestine, gills, and brain also displayed these biotransformation pathways. Cyp3a-like activity was only measurable in liver and intestinal S9 fractions, but all rainbow trout cell lines, including RTgill-W1 and RTbrain, displayed this type of activity. Furthermore, despite RTgutGC having the highest constitutive Cyp3a-like activity, its inducibility was the highest in RTL-W1 cells. Similarly, both RTL-W1 and RTgutGC cells displayed Cyp2b-like activity, but this was only measurable upon induction. Contrarily, S9 fractions from the liver, intestine and gills displayed constitutive Cyp2b-like activity. While these differences could be related to differential functionality of biological processes at the in vivo level, we provide important evidence of a broad spectrum of in vitro enzymatic activity in salmonid models. As such, both S9 fractions and cell lines represent important alternatives to animal testing for evaluating the biotransformation and bioaccumulation of environmental pollutants.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"37"},"PeriodicalIF":5.3,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11775053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051807","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":"HSP27/IL-6 axis promotes OSCC chemoresistance, invasion and migration by orchestrating macrophages via a positive feedback loop.","authors":"Ying Qi, Juan Cao, Mingjing Jiang, Ying Lin, Weibo Li, Bo Li","doi":"10.1007/s10565-024-09983-1","DOIUrl":"10.1007/s10565-024-09983-1","url":null,"abstract":"<p><p>Novel strategies to disrupt tumor progression have emerged from studying the interactions between tumor cells and tumor-associated macrophages (TAMs). However, the molecular mechanisms of interactions between tumor cells and TAMs underlying oral squamous cell carcinoma (OSCC) progression have not been fully elucidated. This study explored the molecular mechanism of the HSP27/IL-6 axis in OSCC chemoresistance, invasion, and migration. Here, we demonstrated the higher expression of HSP27 in OSCC cells. Paracrine HSP27 from OSCC cells enhanced chemoresistance, invasion, migration, and EMT in OSCC by inducing M2 polarization and IL-6 secretion in TAMs. HSP27 and IL-6 established a positive feedback loop between OSCC cells and M2 TAMs. TAMs-derived IL-6 orchestrated OSCC stemness and chemoresistance through upregulating β-catenin and CD44, and enhanced OSCC invasion, migration, and EMT via autocrine HSP27/TLR4 signaling. Collectively, HSP27/IL-6 axis facilitates OSCC chemoresistance, invasion, and migration by orchestrating macrophages through a positive feedback loop. We identify the regulatory mechanism underlying the interaction and crosstalk between OSCC cells and TAMs mediated by the HSP27/IL-6 axis. Targeting the HSP27/IL-6 axis could be a promising treatment strategy for OSCC patients, potentially controlling disease progression and improving prognosis and recurrence outcomes.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"36"},"PeriodicalIF":5.3,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11775009/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058314","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":"Manganese exposure induces parkinsonism-like symptoms by Serpina3n-TFEB-v/p-ATPase signaling mediated lysosomal dysfunction.","authors":"Huihui Hong, Sicheng Liu, Ting Yang, Jinxian Lin, Kun Luo, Yudong Xu, Ting Li, Yu Xi, Lingling Yang, Yuan-Qiang Lu, Wei Yuan, Zhou Zhou","doi":"10.1007/s10565-025-09989-3","DOIUrl":"10.1007/s10565-025-09989-3","url":null,"abstract":"<p><p>Manganese (Mn) is a neurotoxin that has been etiologically linked to the development of neurodegenerative diseases in the case of overexposure. It is widely accepted that overexposure to Mn leads to manganism, which has clinical symptoms similar to Parkinson's disease (PD), and is referred to as parkinsonism. Astrocytes have been reported to scavenge and degrade extracellular α-synuclein (α-Syn) in the brain. However, the mechanisms of Mn-induced neurotoxicity associated with PD remain unclear. Serpina3n is highly expressed in astrocytes and has been implicated in several neuropathologies. The role Serpina3n plays in Mn neurotoxicity and PD pathogenesis is still unknown. Here, we used wild-type and Serpina3n knockout (KO) C57BL/6 J mice with i.p. injection of 32.5 mg/kg MnCl₂ once a day for 6 weeks to elucidate the role of Serpina3n in Mn-caused neurotoxicity regarding parkinsonism pathogenesis. We performed behavioral tests (open field, suspension and pole-climbing tests) to observe Mn-induced motor changes, immunohistochemistry to detect Mn-induced midbrain changes, and Western blot to detect Mn-induced changes of protein expression. It was found that Serpina3n KO markedly alleviated Mn neurotoxicity in mice by attenuating midbrain dopaminergic neuron damage and ameliorating motor deficits. Furthermore, using immunofluorescence colocalization analysis, Western blot and quantitative real-time PCR on Mn-treated C8-D1A cells, we found that Serpina3n KO significantly improved astrocytic α-Syn clearance by suppressing Mn-induced lysosomal dysfunction. Reduced transcription factor EB (TFEB)-v/p-ATPase signaling is responsible for the impairment of the lysosomal acidic environment. These novel findings highlight Serpina3n as a detrimental factor in Mn neurotoxicity associated with parkinsonism, capture the novel role of Serpina3n in regulating lysosomal function, and provide a potential target for antagonizing Mn neurotoxicity and curing parkinsonism in humans.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"34"},"PeriodicalIF":5.3,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759460/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058315","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":"Deciphering SPP1-related macrophage signaling in the pathogenesis of intervertebral disc degeneration.","authors":"Xiao-Jun Yu, Peng Zou, Tian-Qi Li, Xiao-Fan Bai, Shan-Xi Wang, Jian-Bin Guan, Yuan-Ting Zhao, Meng-Wei Li, Xiaodong Wang, Ying-Guang Wang, Ding-Jun Hao","doi":"10.1007/s10565-024-09948-4","DOIUrl":"10.1007/s10565-024-09948-4","url":null,"abstract":"<p><p>This study delved into the molecular mechanisms underlying mechanical stress-induced intervertebral disc degeneration (msi-IDD) through single-cell and high-throughput transcriptome sequencing in mouse models and patient samples. Results exhibited an upsurge in macrophage presence in msi-IDD intervertebral disc (IVD) tissues, with secreted phosphoprotein 1 (SPP1) identified as a pivotal driver exacerbating degeneration via the protein kinase RNA-like endoplasmic reticulum kinase/ activating transcription factor 4/ interleukin-10 (PERK/ATF4/IL-10) signaling axis. Inhibition of SPP1 demonstrated promising outcomes in mitigating msi-IDD progression in both in vitro and in vivo models. These findings underscore the therapeutic promise associated with the modulation of the PERK signaling pathway in IDD, shedding light on the pathogenesis of msi-IDD and proposing a promising avenue for intervention strategies.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"33"},"PeriodicalIF":5.3,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11748470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000765","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":"Innovative treatment of age-related hearing loss using MSCs and EVs with Apelin.","authors":"Shengqun Xu, Dongliang Liu, Fang Zhang, Yuan Tian","doi":"10.1007/s10565-025-09988-4","DOIUrl":"10.1007/s10565-025-09988-4","url":null,"abstract":"<p><p>Utilizing single-cell transcriptome sequencing (scRNA-seq) technology, this study explores the viability of employing mesenchymal stem cells (MSCs) as a therapeutic approach for age-related hearing loss (ARHL). The research demonstrates MSCs' ability to differentiate into inner ear cell subpopulations, particularly hair cells, delivering Apelin via extracellular vesicles (EVs) to promote M2 macrophage polarization. In vitro experiments show reduced inflammation and preservation of hair cell health. In elderly mice, MSCs transplantation leads to hair cell regeneration, restoring auditory function. These findings highlight the regenerative capabilities of MSCs and EV-mediated therapeutic approaches for ARHL.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"31"},"PeriodicalIF":5.3,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11739245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000767","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":"The important role of the histone acetyltransferases p300/CBP in cancer and the promising anticancer effects of p300/CBP inhibitors.","authors":"Xin Wu, Xin Zhang, Shaoshan Tang, Yao Wang","doi":"10.1007/s10565-024-09984-0","DOIUrl":"10.1007/s10565-024-09984-0","url":null,"abstract":"<p><p>Histone acetyltransferases p300 (E1A-associated protein p300) and CBP (CREB binding protein), collectively known as p300/CBP due to shared sequence and functional synergy, catalyze histone H3K27 acetylation and consequently induce gene transcription. p300/CBP over-expression or over-activity activates the transcription of oncogenes, leading to cancer cell growth, resistance to apoptosis, tumor initiation and development. The discovery of small molecule inhibitors targeting p300/CBP histone acetyltransferase activity, bromodomains, dual inhibitors of p300/CBP and BRD4 bromodomains, as well as proteolysis-targeted-chimaera p300/CBP protein degraders, marks significant progress in cancer therapeutics. These inhibitors and degraders induce histone H3K27 deacetylation, reduce oncogene expression and cancer cell proliferation, promote cancer cell death, and decrease tumor progression in mice. Furthermore, p300/CBP inhibitors and protein degraders have been demonstrated to exert synergy when in combination with conventional radiotherapy, chemotherapy and BRD4 inhibitors in vitro as well as in mice. Importantly, two p300/CBP bromodomain inhibitors, CCS1477 and FT-7051, as well as the dual p300/CBP and BRD4 bromodomain inhibitor NEO2734 have entered Phase I and IIa clinical trials in patients with advanced and refractory hematological malignancies or solid tumors. Taken together, the identification of p300/CBP as critical drivers of tumorigenesis and the development of p300/CBP inhibitors and proteolysis-targeted-chimaera protein degraders represent promising avenues for clinical translation of novel cancer therapeutics.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"32"},"PeriodicalIF":5.3,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11742294/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000770","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":"Targeting CHEK1: Ginsenosides-Rh2 and Cu2O@G-Rh2 nanoparticles in thyroid cancer.","authors":"Lidong Wang, Xin Wu, XinLu Wang, Meng Dong, Hao Zhang, Pengfei Zhao","doi":"10.1007/s10565-024-09961-7","DOIUrl":"10.1007/s10565-024-09961-7","url":null,"abstract":"<p><p>Thyroid cancer (THCA) is an increasingly common malignant tumor of the endocrine system, with its incidence rising steadily in recent years. For patients who experience recurrence or metastasis, treatment options are relatively limited, and the prognosis is poor. Therefore, exploring new therapeutic strategies has become particularly urgent. This study confirmed that effective suppression of THCA cell proliferation and stimulation of apoptosis can be achieved through the application of Ginsenosides-Rh2. Through network pharmacology screening, the molecular target of Ginsenosides-Rh2 in THCA was identified as CHEK1, and its inhibitory effect was confirmed by downregulating CHEK1 protein expression. Furthermore, demonstrations conducted both in vitro and in vivo showcased that delivering Ginsenosides-Rh2 using nanoparticle carriers significantly reduced cell viability by approximately 50%, regulated DNA damage levels, apoptosis-related protein expression, and cell cycle control. The IC50 of the nanoparticle formulation was determined (B-CPAP IC50 = 88.24 μM), TPC IC50 = 79.52 μM). This study confirmed that Cu2O@G-Rh2 is effective in suppressing tumors and exhibits a significant inhibitory effect on tumor recurrence and metastasis while maintaining good safety. Cu2O@G-Rh2 nanoparticles possess excellent stability and anti-tumor efficacy. This research offers new perspectives for the treatment of THCA and demonstrates potential clinical applications.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"30"},"PeriodicalIF":5.3,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11732901/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142977874","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}