Journal of The American Society of Nephrology最新文献

{"title":"Correction: The RNA-Protein Interactome of Differentiated Kidney Tubular Epithelial Cells.","authors":"Ignarski Michael,Rill Constantin,W J Kaiser Rainer,Kaldirim Madlen,Neuhaus René,Esmaillie Reza,Li Xinping,Klein Corinna,Bohl Katrin,Petersen Maike,Frese Christian K,Höhne Martin,Atanassov Ilian,Rinschen Markus M,Höpker Katja,Schermer Bernhard,Benzing Thomas,Dieterich Christoph,Fabretti Francesca,Müller Roman-Ulrich","doi":"10.1681/asn.0000000737","DOIUrl":"https://doi.org/10.1681/asn.0000000737","url":null,"abstract":"","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":"5 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143824820","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":"Insulin-Like Growth Factor-Binding Protein 7 and Cadmium-Induced Hepatorenal Fibrosis.","authors":"Shuai-Shuai Xie,Rui Hou,Li Gao,Qin Yang,Wei Li,Ze-Hui Dong,Yu-Hang Dong,Shuang-Jian Li,Wen-Xian Ma,Ying-Ying Gao,Long Xu,Chao Li,Ying Chen,Ju-Tao Yu,Jia-Nan Wang,Ming-Lu Ji,Ruo-Bing He,Xiao-Guo Suo,Ming-Ming Liu,Juan Jin,Jia-Gen Wen,Chen Yang,Xiao-Ming Meng","doi":"10.1681/asn.0000000698","DOIUrl":"https://doi.org/10.1681/asn.0000000698","url":null,"abstract":"BACKGROUNDChronic cadmium exposure can induce the onset and progression of hepatorenal fibrosis; however, its molecular basis is unclear. Insulin-like growth factor-binding protein 7 (IGFBP7) is not only a biomarker of acute kidney injury (AKI), but also plays a functional role in promoting kidney injury and inflammation. Abnormal repair of AKI causes kidney fibrosis and chronic kidney disease. IGFBP7 has also been reported as a more sensitive biomarker for liver fibrosis. However, its role in hepatorenal fibrosis requires further investigation.METHODSIGFBP7 global and conditional knockout mice were used to determine the role of IGFBP7 in cadmium-induced hepatorenal fibrosis. Then, liquid chromatography-mass spectrometry, truncated mutants, co-immunoprecipitation, and microscale thermophoresis were employed to unravel the downstream mechanisms.RESULTSIGFBP7 expression was significantly elevated in kidney and liver tissues of mice subjected to chronic cadmium exposure. IGFBP7 deficiency attenuated cadmium-induced hepatorenal dysfunction and fibrosis, whereas restoration of IGFBP7 expression in IGFBP7-deficient mice reproduced hepatorenal fibrosis. Mechanistically, IGFBP7 interacted with alpha-enolase (ENO1) and inhibited its ubiquitination and degradation. Upregulated ENO1 further promoted glucose metabolic reprogramming and lactate accumulation. Conversely, lactate accumulation enhanced IGFBP7 transcription and expression through histone H3K18 lactylation. Importantly, therapy targeting IGFBP7 significantly ameliorated cadmium-induced hepatorenal fibrosis.CONCLUSIONSIGFBP7 promoted cadmium-induced hepatorenal fibrosis by enhancing ENO1-driven abnormal glycolysis and lactate accumulation.","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":"10 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819376","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":"Noninvasive Diagnosis of Acute Tubulointerstitial Nephritis in Clinical Practice.","authors":"Marimar Contreras Nieves,Shuchi Anand","doi":"10.1681/asn.0000000694","DOIUrl":"https://doi.org/10.1681/asn.0000000694","url":null,"abstract":"","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":"33 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819058","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":"Tubular Cell Polyploidy and AKI-to-CKD Transition.","authors":"Elena Lazzeri,Paola Romagnani","doi":"10.1681/asn.0000000696","DOIUrl":"https://doi.org/10.1681/asn.0000000696","url":null,"abstract":"","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":"23 17 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143818981","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":"Association of Clonal Hematopoiesis of Indeterminate Potential with Cardiovascular Events in Patients with CKD.","authors":"Yang Pan,Caitlyn Vlasschaert,Varun Rao,Elvis A Akwo,James E Hixson,Mesbah Uddin,Zhi Yu,Do-Kyun Kim,Alexander Bick,Bryan Kestenbaum,Michael Chong,Guillaume Paré,Michael Rauh,Adeera Levin,James P Lash,Manjula Kurella Tamura,Debbie L Cohen,Jiang He,Lee Hamm,Rajat Deo,Zeenat Bhat,Panduranga Rao,Dawei Xie,Pradeep Natarajan,Tanika N Kelly,Cassianne Robinson-Cohen,Matthew B Lanktree,","doi":"10.1681/asn.0000000671","DOIUrl":"https://doi.org/10.1681/asn.0000000671","url":null,"abstract":"BACKGROUNDPatients with CKD are at higher risk of cardiovascular disease. Clonal hematopoiesis of indeterminate potential (CHIP) has been associated with cardiovascular disease in the general population, with a causal role observed in animal models. In the general population, the effect of CHIP is greater for somatic mutations in pre-defined CHIP driver genes other than DNMT3A (referred to as non-DNMT3A CHIP). We sought to assess the prospective association between CHIP and cardiovascular events in patients with CKD.METHODSCHIP was measured by high-depth targeted sequencing. The primary analysis tested the association of somatic mutations in non-DNMT3A CHIP driver genes with a composite cardiovascular disease endpoint of myocardial infarction, stroke, congestive heart failure, and peripheral artery disease in 5,043 patients with CKD in four prospective cohorts. Sensitivity analyses examined the effect of CHIP subtypes, race, baseline comorbidities, APOL1 risk alleles, and IL6R p.Asp358Ala genotype.RESULTSAt baseline, patients had a mean age of 66 ± 12 years and eGFR of 43 ± 18 ml/min/1.73m2. CHIP was present in 24% of patients, with 13% of all patients carrying acquired non-DNMT3A mutations. Non-DNMT3A CHIP was associated with a 36% higher risk of the composite cardiovascular endpoint [95% confidence interval (CI), 6% - 76%]. Among composite components, non-DNMT3A CHIP was associated with a higher risk of stroke (HR 1.65; 95% CI 1.10 - 2.47). Baseline eGFR, diabetes status, or race did not alter the association of non-DNMT3A CHIP with cardiovascular risk. Those without genetically reduced interleukin-6 signaling (non-carriers of IL6R p.Asp358Ala) had worse disease (HR 1.46; 95% CI 1.17- 1.83, Psubgroup difference = 0.05).CONCLUSIONSIn patients with CKD, non-DNMT3A CHIP was associated with cardiovascular disease with an effect size similar to that reported in the general population.","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":"65 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819133","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":"Clonal Hematopoiesis of Indeterminate Potential and Progression of CKD.","authors":"Caitlyn Vlasschaert,Yang Pan,Jianchun Chen,Elvis Akwo,Varun Rao,James E Hixson,Michael Chong,Md Mesbah Uddin,Zhi Yu,Mengdi Jiang,Fenfen Peng,Shirong Cao,Yinqiu Wang,Do-Kyun Kim,Adriana M Hung,Jing He,Manjula Kurella Tamura,Debbie L Cohen,Jiang He,Changwei Li,Zeenat Bhat,Panduranga Rao,Dawei Xie,Alexander G Bick,Bryan Kestenbaum,Guillaume Paré,Michael J Rauh,Adeera Levin,Pradeep Natarajan,James P Lash,Ming-Zhi Zhang,Raymond C Harris,Cassianne Robinson-Cohen,Matthew B Lanktree,Tanika N Kelly,","doi":"10.1681/asn.0000000680","DOIUrl":"https://doi.org/10.1681/asn.0000000680","url":null,"abstract":"BACKGROUNDClonal hematopoiesis of indeterminate potential (CHIP) is a common inflammatory condition of aging that causes myriad end-organ damage. CHIP has been associated with incident AKI and kidney function decline in the general population, particularly mutations in CHIP genes other than DNMT3A (termed non-DNMT3A CHIP). Prior studies of CHIP in individuals with CKD had limited sample sizes and conflicting findings.METHODSWe examined CHIP and CKD progression in four CKD cohorts (N = 5,654): the Chronic Renal Insufficiency Cohort (CRIC), the African American Study of Kidney Disease (AASK), individuals with CKD from the BioVU biorepository, and the Canadian study of prediction of death, dialysis and interim cardiovascular events (CanPREDDICT).Primary outcomes were incident CKD progression (50% eGFR decline or kidney failure), and eGFR slope over time. In addition, kidney function and pathology were assessed in a Tet2-CHIP mouse model of CKD induced by dietary adenine.RESULTSAcross all cohorts the average age was 66 ± 11 years, with an average baseline eGFR of 43 ± 15 ml/min/1.73m2, and 24% had CHIP. After meta-analysis, non-DNMT3A CHIP was associated with a 64% higher relative risk of incident CKD progression (hazard ratio [HR] 1.64; 95% confidence interval [CI], 1.00-2.68), with the strongest effect observed in individuals with baseline eGFR 30-60 ml/min/1.73m2 (HR 1.85, 95% CI: 1.18-2.90). Non-DNMT3A CHIP carriers also exhibited a faster eGFR decline (β, -0.62 ± 0.28 ml/min/1.73m2 per year; P = 0.03). In a dietary adenine mouse model of CKD, Tet2-CHIP was associated with lower GFR as well as greater kidney inflammation, tubular injury, and tubulointerstitial fibrosis.CONCLUSIONSNon-DNMT3A CHIP was associated with CKD progression among individuals with CKD. Further, Tet2-CHIP mouse models support a causal role in kidney injury.","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":"25 1","pages":""},"PeriodicalIF":13.6,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819074","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":"Drug-Induced Membranous Nephropathy: Piecing Together Clues to Understand Disease Mechanisms.","authors":"Rupali S Avasare, Nicole K Andeen, Laith F Al-Rabadi, Kevin Burfeind, Laurence Beck","doi":"10.1681/ASN.0000000719","DOIUrl":"https://doi.org/10.1681/ASN.0000000719","url":null,"abstract":"<p><strong>Abstract: </strong>There is a resurgence of interest in drug-induced membranous nephropathy due to the widespread availability of recently discovered culprit medications, such as lipoic acid supplements, mercury in skin lightening creams, and nonsteroidal anti-inflammatory drugs (NSAIDs) and the relationship between these drugs and newly described target antigens. The clinical syndromes associated with drug-induced membranous nephropathy are similar in that proteinuria ranges from low-grade to nephrotic-range and generally remits within months of drug cessation. Histology is notable for subepithelial deposits that are immunoglobulin G1 (IgG1) subclass predominant, sometimes with a unique segmental distribution. The two antigens associated with drug-induced membranous nephropathy are neural epidermal growth factor-like 1 (NELL1) and proprotein convertase subtilisin/kexin 6 (PCSK6). Notably, several of the culprit drugs contain one or more sulfhydryl groups that may have potential mechanistic relevance. Here we review past research investigations into mechanisms of membranous nephropathy associated with gold salts, penicillamine, and mercury and use these historical studies as the basis for formulating new hypotheses on how drugs might promote immune dysregulation and, ultimately, membranous nephropathy.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":10.3,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811667","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":"Volume Assessment in Patients Undergoing Long-Term Dialysis.","authors":"Benjamin Lazarus, Simon J Davies, Kevan R Polkinghorne","doi":"10.1681/ASN.0000000724","DOIUrl":"https://doi.org/10.1681/ASN.0000000724","url":null,"abstract":"<p><strong>Abstract: </strong>Accurate assessment of fluid status is a priority for patients with kidney failure undergoing long-term dialysis. There is wide variation in current volume-related practices between dialysis units and an urgent need to develop better evidence to guide practice. Clinical decisions relating to volume management are implicitly based on assessment of volume status, and there are numerous different but imperfect methods of assessment. Isotope-based dilutions are impractical for clinical use and may not be a gold-standard for patients with kidney failure. Individual trends in body weight and blood pressure have been used as a pragmatic surrogate marker for volume status. Probing the target weight based on blood pressure is still widely practiced but may pose risks related to volume depletion and accelerated loss of residual kidney function. Clinical signs such as elevated jugular venous pressure and leg edema are readily accessible but have poor diagnostic accuracy and wide interobserver variability that limit their reproducibility for volume assessment in clinical trials. Lung ultrasound and bioelectrical impedance analysis have a sound scientific rationale for the assessment of extracellular volume, and are appropriately associated with clinical outcomes, but neither approach has demonstrated convincingly favorable clinical outcomes in clinical trials. Other technologies for volume assessment exist but require further assessment in clinical trials. Advancements in clinical care can be made with existing technologies through comparative effectiveness trials of different fluid management strategies, routine and standardized measurement of volumetric parameters and individual patient preferences, and innovative integration of existing volume assessment methods. A systematic and globally coordinated approach to improving volume assessment and management is required to improve outcomes in patients receiving long-term dialysis.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":10.3,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143795947","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":"Alterations in DNA Methylation, Proteomic, and Metabolomic Profiles in African Ancestry Populations with APOL1 Risk Alleles.","authors":"Xinruo Zhang, Ashley W Scadden, Amarnath Marthi, Victoria L Buchanan, Yishu Qu, Kendra R Ferrier, Brian D Chen, Mariaelisa Graff, Julian Avila, Eric Boerwinkle, Steve Buyske, Clary B Clish, Dan Cruz, Myriam Fornage, Robert E Gerzsten, Christopher R Gignoux, LaShaunta Glover, Lifang Hou, Anne E Justice, Charles Kooperberg, Holly Kramer, Leslie Lange, Ruth J F Loos, Tara Matise, Josyf C Mychaleckyj, Opeyemi A Olabisi, Ulrike Peters, Laura M Raffield, Alex P Reiner, Stephen S Rich, Jerome I Rotter, Kent D Taylor, Bing Yu, Yinan Zheng, Kari E North, Amy K Mottl, Heather M Highland, Maggie A Stanislawski","doi":"10.1681/ASN.0000000688","DOIUrl":"https://doi.org/10.1681/ASN.0000000688","url":null,"abstract":"<p><strong>Background: </strong>The APOL1 high-risk haplotype has been associated with chronic kidney disease (CKD) and the deterioration of kidney function, particularly in populations with West African ancestry. However, the mechanisms by which APOL1 risk variants increase the risk for kidney disease and its progression have not been fully elucidated.</p><p><strong>Methods: </strong>We compared methylation (N = 3,191; 715 [22%] carriers), proteomic (N = 1,240; 169 [14%] carriers), and metabolomic (N = 6,309; 674 [11%] carriers) profiles in African and Hispanic/Latino carriers of two APOL1 high-risk alleles (G1/G1, G2/G2, G1/G2) and non-carriers (G0/G0), excluding heterozygotes (G0/G1, G0/G2), from the PAGE Consortium and UK BioBank. In each study, the associations between the APOL1 high-risk haplotype and up to 722,719 CpG sites, 2,923 proteins, or 836 metabolites were estimated using covariate-adjusted linear regression models, followed by fixed-effects sample size weighted meta-analyses.</p><p><strong>Results: </strong>Significant associations were observed between APOL1 high-risk haplotype and methylation at 52 CpG sites, with 48 located on chromosome 22 and 18 in the vicinity of APOL1 - 4 and MYH9. All significant CpG sites near APOL2 were hypomethylated, whereas those near APOL3 and APOL4 were hypermethylated. APOL1-associated CpG sites were also identified in genes involved in ion transport and mitochondrial stress pathways. Sensitivity analyses indicated consistent yet attenuated effects among heterozygotes, supporting an additive effect of APOL1 risk alleles. Further analyses of the 52 CpG sites identified two near APOL4 exhibiting G1-specific effects, eight associated with CKD but none with eGFR, and three showing heterogeneity by CKD status. Additionally, carrying two APOL1 risk alleles was associated with higher plasma APOL1 protein (β = 1.12, PFDR = 2.26e-70) and lower C18:1 cholesteryl ester metabolite (Z = -4.50, PFDR = 4.83e-3).</p><p><strong>Conclusions: </strong>Our results demonstrate differential methylation, proteomic, and metabolomic profiles associated with APOL1 high-risk haplotypes.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":10.3,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143795939","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":"Late Allograft Loss and Contemporary Cardio-Renal Metabolic Therapies.","authors":"Amanda J Vinson, Arthur Matas","doi":"10.1681/ASN.0000000726","DOIUrl":"https://doi.org/10.1681/ASN.0000000726","url":null,"abstract":"<p><strong>Abstract: </strong>Late kidney allograft loss occurs through one of two mechanisms: a) deterioration of kidney function leading to re-transplantation or dialysis (death-censored graft loss) and b) premature death with a normally functioning transplant (death with graft function) -each accounting for approximately 50% of late kidney graft losses. Late death-censored graft loss typically results from a combination of immune and nonimmune events leading to common nonspecific endpoints (e.g., tubular atrophy, interstitial fibrosis and glomerulosclerosis). Conversely, leading causes of death with graft function typically include cardiovascular events, malignancy, and infection. With an improved understanding of the multiple mechanism by which late graft dysfunction develops, there is an opportunity to identify patients at greatest risk and institute novel strategies to quell the process. Newer cardiometabolic agents with proven benefit in the general population have not been well-studied in kidney transplant recipients. However, in addition to their potential benefits in terms of reducing cardiovascular, infectious and malignancy endpoints (thus minimizing death with graft function risk), many novel agents may have additional anti-inflammatory and/or anti-fibrotic benefit (minimizing death-censored graft loss risk) in the kidney transplant population. In this review, we summarize existing literature regarding major causes of death-censored graft loss and death with graft function, and discuss the potential roles of new cardio-renal metabolic agents including sodium-glucose cotransport 2 inhibitors (SGLT2i), non-steroidal mineralocorticoid receptor antagonists (MRA), glucagon-like peptide 1 receptor agonists (GLP1-RA), and dual endothelin and angiotensin receptor antagonists in the kidney transplant population, including potential mechanisms to improve death with graft function and death-censored graft loss outcomes.</p>","PeriodicalId":17217,"journal":{"name":"Journal of The American Society of Nephrology","volume":" ","pages":""},"PeriodicalIF":10.3,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143795945","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}