Circulation最新文献

{"title":"Letter by Luo et al Regarding Article, \"Screening-Detected Atrial Fibrillation and Cardiovascular Outcomes in Working-Age Adults\".","authors":"Yunhe Luo,Jing Zhao,Qiang Dong","doi":"10.1161/circulationaha.125.077870","DOIUrl":"https://doi.org/10.1161/circulationaha.125.077870","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"22 1","pages":"e1126-e1127"},"PeriodicalIF":37.8,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147726231","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":"Inflammatory Hot Phases and Disease Trajectory in Desmosomal Cardiomyopathies.","authors":"Andrea Mazzanti,Deni Kukavica,Silvia G Priori","doi":"10.1161/circulationaha.125.078652","DOIUrl":"https://doi.org/10.1161/circulationaha.125.078652","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"22 1","pages":"1179-1181"},"PeriodicalIF":37.8,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147725990","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":"Response by Gasperetti et al to Letter Regarding Article, \"Prognostic Role of Myocarditis-Like Episodes and Their Treatment in Patients With Pathogenic Desmoplakin Variants\".","authors":"Alessio Gasperetti,Giovanni Peretto,Cynthia A James,Maurizio Pieroni,Adam S Helms,Hugh Calkins,Nisha A Gilotra","doi":"10.1161/circulationaha.126.079059","DOIUrl":"https://doi.org/10.1161/circulationaha.126.079059","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"135 1","pages":"e1124-e1125"},"PeriodicalIF":37.8,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147725989","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":"Pressure Overload-Induced Ventricular Crosstalk Activates Regenerative Mechanisms in the Contralateral Ventricle in Neonatal Mice.","authors":"Fabian Ebach,Julia Nicke,Tianyuan Hu,Hemmen Sabir,Andreas Müller,Bernd K Fleischmann,Mona Malek Mohammadi","doi":"10.1161/circulationaha.125.077779","DOIUrl":"https://doi.org/10.1161/circulationaha.125.077779","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"9 1","pages":"1261-1264"},"PeriodicalIF":37.8,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147726022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting E3 Ubiquitin Ligase Hrd1 Prevents Myocardial Ischemia-Reperfusion Injury Through Enhancing ALDH2 Enzymatic Activity.","authors":"Liu Shuolin,Li Chuanyin,Min Zhu,Tingfang Zhu,Yiran E Li,Yanlin Liu,Chenguo Xu,Hongyan Wang,Ronggui Hu,Junbo Ge,Yingmei Zhang","doi":"10.1161/circulationaha.125.074399","DOIUrl":"https://doi.org/10.1161/circulationaha.125.074399","url":null,"abstract":"BACKGROUNDMyocardial ischemia-reperfusion (I/R) injury presents a significant clinical challenge characterized by a complex pathological mechanism. The role of protein ubiquitination in I/R injury has not been systematically investigated. Global ubiquitinome profiling was conducted to identify the potential key players in myocardial I/R injury.METHODSThe ubiquitination levels of proteins in mouse hearts subjected to either sham surgery or I/R injury were analyzed using ubiquitinome. A combined analysis of ubiquitinome, single-cell RNA sequencing (RNA-seq), and proteomics data was employed to predict potential E3 ubiquitin ligases associated with myocardial I/R injury. Global heterozygous 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase degradation 1 (Hrd1) knockout, endothelial cell (EC)-specific Hrd1 deficiency (Hrd1f/f; Cdh5Cre), and EC-specific Hrd1 overexpression (AAV-EC-Hrd1) mice were used to assess the role of Hrd1 in myocardial I/R injury. Mass spectrometry and immunoprecipitation were used to elucidate the interaction between Hrd1 and aldehyde dehydrogenase 2 (ALDH2). Additionally, we assessed ubiquitination and vasomotor reactivity to clarify the mechanisms by which Hrd1 regulates ALDH2 activity and EC dysfunction during I/R injury.RESULTSUbiquitinome analysis revealed that protein ubiquitination exacerbates endothelial dysfunction after myocardial I/R injury. Integrative analysis of the ubiquitinome, proteomics, and single-cell RNA-seq revealed a significant upregulation of the E3 ubiquitin-protein ligase Hrd1 in CD45+ ECs. In both humans and mice, the level of endothelial Hrd1 protein was found to increase in response to I/R in vivo. Genetic ablation of Hrd1 significantly alleviated myocardial infarction, endothelial dysfunction, and infiltration of inflammatory cells after I/R injury. Mechanistically, Hrd1 promoted the K33-linked polyubiquitination of ALDH2 and then inhibited the formation of its active tetramers, which reduced the apoptosis of CD45+ ECs and exacerbated endothelial dysfunction through the NO/cGMP/PKG (nitric oxide-cyclic guanosine monophosphate-protein kinase G) signaling pathway. Furthermore, our findings demonstrated that pharmacological inhibition of Hrd1 robustly ameliorated myocardial I/R injury and endothelial dysfunction.CONCLUSIONSOur findings demonstrated a previously unidentified crucial role of cardiac EC Hrd1 in myocardial I/R injury. Hrd1 may serve as a therapeutic target for preventing myocardial I/R injury.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"5 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147695161","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":"The Natural History of Massive Left Ventricular Hypertrophy in Pediatric Hypertrophic Cardiomyopathy: A Multiregistry Analysis.","authors":"Robert Przybylski,Gabrielle Norrish,Brian Claggett,Euan A Ashley,Vinay Bhole,Sharlene M Day,Grazia Delle Donne,Adrian Fernandez,Francesca Girolami,Belinda Gray,Adam S Helms,Jodie Ingles,Peter Kubus,Neal K Lakdawala,Rachel J Lampert,Kimberly Y Lin,Michelle Michels,Erin Miller,Iacopo Olivotto,Anjali Owens,Victoria N Parikh,Silvia Passantino,Cristina Ramona Radulescu,Joseph Rossano,Mark W Russell,Thomas D Ryan,Sara Saberi,Georgia Spentzou,John C Stendahl,James S Ware,Robert G Weintraub,Lidia Ziolkowska,Peter-Paul Zwetsloot,Juan Pablo Kaski,Carolyn Y Ho,Dominic J Abrams, ","doi":"10.1161/circulationaha.126.078843","DOIUrl":"https://doi.org/10.1161/circulationaha.126.078843","url":null,"abstract":"BACKGROUNDMassive left ventricular hypertrophy (LVH) is a risk factor for sudden cardiac death in children with hypertrophic cardiomyopathy (HCM), but little is understood about its natural history.METHODSPatients with pediatric-onset HCM identified from 2 registries (SHaRe [Sarcomeric Human Cardiomyopathy Registry] and IPHCC [International Paediatric Hypertrophic Cardiomyopathy Consortium]) with or without massive LVH were compared. Massive LVH was defined as absolute maximal left ventricular wall thickness (MLVWT) ≥30 mm or MLVWT z score ≥+20 at <18 years of age. Data from SHaRe and IPHCC include encounters from January 1960 through March 2024 and January 1970 through March 2024, respectively. Demographic, clinical, and serial MLVWT data were collected. Composite outcomes included major ventricular arrhythmia event (sudden cardiac death, aborted sudden cardiac death, or appropriate implantable cardioverter defibrillator therapy); heart failure (HF) event (left ventricular ejection fraction <50%, New York Heart Association class III or IV, transplant, or HF-related death); major adverse cardiac event (stroke or any major ventricular arrhythmia or HF outcome aside from left ventricular ejection fraction <50%); and HCM-related mortality (sudden cardiac death or HF-related death). Time-to-event analyses were performed using Cox proportional hazards models.RESULTSWe identified 587 patients (54 female [30%]). In 186 children with massive LVH, age at diagnosis was younger (median, 9.2 years [interquartile range, 2.1-13.1 years]) versus 13.6 years (9.7-15.5 years; P<0.001) and sarcomeric genetic variants more prevalent (72% versus 61%; P=0.034), as was HCM-related mortality (unadjusted hazard ratio, 3.3 [95% CI,1.2-9.7]; P=0.026), major adverse cardiac events (hazard ratio, 2.6 [1.7-3.9]; P<0.001), major ventricular arrhythmia (hazard ratio, 3.1 [1.8-5.2]; P<0.001), and HF (hazard ratio, 1.9 [1.1-3.1]; P=0.013). These associations remained significant when adjusted for sex and age at HCM diagnosis. In 115 patients with massive LVH with serial MLVWT data (62%), MLVWT increased significantly from first to last measurements (median, 26 mm [interquartile range, 18-32 mm] versus 31 mm [26-35 mm]; P<0.001), but there was no difference between z scores (median, +22 [interquartile range, +18 to +26] versus +23 [+20 to +28]; P=0.25). The last absolute MLVWT recorded was >5 mm less than the largest recorded MLVWT in 25 patients (22%).CONCLUSIONSIn pediatric HCM, massive LVH disproportionately affects those diagnosed in early childhood with sarcomeric disease, with increased risk for adverse events. Significant MLVWT regression is seen in nearly a quarter of patients.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"8 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147695160","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":"WNT5a-Mediated Aberrant Actin Filament Dynamics Drive Cardiac Pathogenic Phenotypes in LMNA-Related Emery-Dreifuss Muscular Dystrophy.","authors":"Hangping Fan,Xiaochen Wang,Xujie Liu,Jiuxiao Zhao,Yuan Zhang,Zongkuai Yang,Hao Wang,Junhao Gong,Lingying Li,Jiamin Jin,Yuxuan Guo,Tingyu Gong,Lenan Zhuang,Qing Ke,Ping Liang","doi":"10.1161/circulationaha.125.075604","DOIUrl":"https://doi.org/10.1161/circulationaha.125.075604","url":null,"abstract":"BACKGROUNDEmery-Dreifuss muscular dystrophy (EDMD) is a rare genetic disorder characterized by early-onset joint contractures, progressive muscle atrophy, and cardiac abnormalities. Patients with EDMD carrying LMNA sequence variations often exhibit severe cardiac manifestations, including frequent atrioventricular block and ventricular tachycardia. Approximately 20% of those patients may ultimately require heart transplantation. The molecular mechanisms by which LMNA sequence variations lead to EDMD remain unknown.METHODSFive clinically diagnosed patients with EDMD carrying LMNA sequence variations were recruited. Patient-specific induced pluripotent stem cells (iPSCs) were generated using a nonintegrating Sendai virus. Previously generated iPSCs, derived from 2 healthy donors, were used as controls. The LMNA L204P sequence variation was corrected by genome editing in EDMD iPSC lines to generate isogenic controls. All iPSC-derived cardiomyocytes (iPSC-CMs) were generated using a monolayer-based differentiation protocol. Three-dimensional, strip-format, and force-generating human engineered heart tissues were generated from iPSC-CMs. A knock-in mouse model carrying the Lmna L204P sequence variation was also generated.RESULTSEDMD-specific iPSC-CMs exhibited a variety of deleterious phenotypes, including disorganized sarcomeres, abnormal nuclear envelope structure, arrhythmias, and contractile dysfunction, when compared with control and gene-corrected iPSC-CMs. Multi-omics analysis further revealed that LMNA directly binds the WNT5A promoter and the Leu204Pro sequence variation reduces chromatin accessibility and WNT5A transcription in EDMD iPSC-CMs. WNT5a (Wnt family member 5a)/RhoA (Ras homolog family member A) signaling inactivation was shown to lead to actin depolymerization and inhibition of actin polymerization in EDMD iPSC-CMs. This results in a deformed nuclear envelope, contractile dysfunction, and impaired trafficking of Cx43 (connexin 43). The impairment of Cx43 trafficking causes reduced distribution of Cx43 at cell-cell borders, contributing to the arrhythmic phenotype in EDMD iPSC-CMs. Pharmacological interventions of exogenous WNT5a supplementation, RhoA activator, or an actin polymerization stabilizer effectively rescued the pathogenic phenotypes of EDMD iPSC-CMs. EDMD engineered heart tissues displayed dysfunctional contractile force generation, which was significantly alleviated by RhoA activator. Lmna L204P heterozygous knock-in mice exhibited impaired cardiac function and developed cardiac arrhythmias in response to sympathetic stress.CONCLUSIONSWe present WNT5a-mediated aberrant actin filament dynamics as a novel mechanism underlying cardiac pathogenic phenotypes in LMNA-related EDMD. Our findings indicate that activating WNT5a/RhoA and stabilizing actin assembly may serve as novel therapeutic strategies for this condition.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"22 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147695166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Interleukin-8-Mediated Cellular Crosstalk Reverses Hypertrophic Cardiomyopathy and Cardiac Fibrosis in Noonan Syndrome.","authors":"Jakob Fell,Mario Pavez-Giani,Fabian Koitka,George Kensah,Gabriela Leao Santos,Emiel P C van der Vorst,Christof Lenz,Gabriela Salinas,Alexandra Victoria Busley,Alisa Fedorenko,Robin Hindmarsh,Cordula Maria Wolf,Susanne Lutz,Gerd Hasenfuss,Wolfram-Hubertus Zimmermann,Bernd Wollnik,Lukas Cyganek","doi":"10.1161/circulationaha.125.074155","DOIUrl":"https://doi.org/10.1161/circulationaha.125.074155","url":null,"abstract":"BACKGROUNDGenetic variants in components or regulators of the RAS-MAPK signaling pathway are causative for severe and early-onset hypertrophic cardiomyopathy (HCM) in patients with Noonan syndrome (NS). Despite paracrine communication being considered to play a pivotal role in the etiology of cardiomyopathies, there is a paucity of knowledge about the underlying pathomechanism that leads to the development of hypertrophic cardiomyopathy and cardiac fibrosis in NS.METHODSTo dissect the impact of noncardiomyocytes in the development of NS, we employed two-dimensional and three-dimensional human induced pluripotent stem cell models of LZTR1 deficiency alongside induced pluripotent stem cells derived from patients with NS with pathogenic variants in key RAS-MAPK genes and analyzed these cells and tissues at the molecular, cellular, and functional levels.RESULTSOur findings revealed that cytokine-mediated cellular crosstalk between cardiac fibroblasts and cardiomyocytes, predominantly activated in the disease state, serves as a primary driver of the disease. Cardiac fibroblast-specific IL-8 (interleukin-8) secretion induced fibrosis-related signatures, tissue stiffness, cardiomyocyte hypertrophy, and hypercontractility, identifying dysregulated IL-8 as a heart-autonomous signaling molecule independent of inflammation and immune cell involvement. Inhibition of IL-8-CXCR1 signaling by reparixin reversed the pathological effects in cardiac fibroblasts and cardiomyocytes.CONCLUSIONSThese data provide evidence that targeting aberrant IL-8-CXCR1 signaling may be an effective therapeutic option for patients with NS-associated hypertrophic cardiomyopathy.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"5 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147685096","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":"Highlights From the <i>Circulation</i> Family of Journals.","authors":"","doi":"10.1161/CIRCULATIONAHA.126.080437","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.126.080437","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"153 15","pages":"1165-1170"},"PeriodicalIF":38.6,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147670951","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 Resistance Compromises the Pentose Phosphate Pathway and Impairs Left Ventricular Assist Device-Mediated Myocardial Recovery in Obese Patients With Heart Failure.","authors":"Tuo Pan, Tianyu Liu, Chenyu Jiang, Xiafeng Yu, Yuxi Ji, Jian Liu, Yi Shen, Xingliang Zhou, Yi Yan, Bei Feng, Li Xiang, Erjun Zhu, Qiang Wang, Baowei Shao, Dihao Pan, Liang Ma, Xiangyang Xu, Yanjun Sun, Lin Han, Dongjin Wang, Yiwei Liu, Hao Zhang","doi":"10.1161/CIRCULATIONAHA.124.072850","DOIUrl":"10.1161/CIRCULATIONAHA.124.072850","url":null,"abstract":"<p><strong>Background: </strong>End-stage heart failure (HF) remains a major global health challenge, and left ventricular assist devices (LVADs) represent an important therapeutic option. LVAD-mediated mechanical unloading improves cardiac function and promotes myocardial recovery in many patients with HF; however, this recovery response is suboptimal in obese patients. The mechanisms by which LVAD-mediated unloading induces myocardial recovery, and how obesity alters these processes to blunt myocardial recovery, remain poorly understood.</p><p><strong>Methods: </strong>Patients with HF receiving LVAD support were recruited to investigate the correlation between patients' body mass index and the myocardial recovery response following LVAD implantation. In parallel, a mouse model of heterotopic cervical heart transplantation was used to simulate LVAD-mediated cardiac unloading. Single-nucleus RNA sequencing and stable-isotope tracing metabolomics were performed to explore the changes of signaling pathways and metabolic processes in unloaded hearts. In vitro cyclic stretch assays were used to evaluate how reduced mechanical load regulates cardiomyocyte metabolic pathways. Unloaded hearts from HF mice were used to determine whether the identified metabolic processes contribute to unloading-induced myocardial recovery. Furthermore, the unloaded hearts from obese HF mice were used to evaluate whether these metabolic adaptations are attenuated by obesity.</p><p><strong>Results: </strong>HF patients with a higher body mass index (≥28.0) and greater insulin resistance tended to have poorer LVAD-mediated myocardial recovery. Single-nucleus RNA sequencing showed that mechanical unloading activated myocardial insulin signaling and increased glucose uptake. Stable-isotope tracing metabolomics further revealed that glucose taken up by unloaded hearts was preferentially shunted into the pentose phosphate pathway. Mechanistically, reduced mechanical stress attenuated Hippo pathway activation in cardiomyocytes, facilitating insulin signaling and enhancing pentose phosphate pathway flux. In unloaded hearts from HF mice, increased pentose phosphate pathway flux could reduce oxidative stress and exert cardioprotective effects. However, these benefits were blunted by insulin resistance in obese mice, whereas treatment with insulin sensitizers alleviated insulin resistance and restored unloading-mediated cardioprotection.</p><p><strong>Conclusions: </strong>In failing hearts, mechanical unloading leads to activation of insulin signaling, resulting in increased glucose uptake and enhanced pentose phosphate pathway flux to protect cardiomyocytes against oxidative stress. However, this cardioprotective effect is attenuated by obesity-induced insulin resistance. Administration of insulin sensitizers has the potential to improve LVAD-mediated myocardial recovery in obese patients with HF.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1141-1164"},"PeriodicalIF":38.6,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146124075","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}