Cardiovascular Research最新文献

{"title":"Atrial fibrillation: a measure from one circular RNA.","authors":"Francesco Ruberto,Roger Foo","doi":"10.1093/cvr/cvaf083","DOIUrl":"https://doi.org/10.1093/cvr/cvaf083","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"12 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144097729","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":"Novel roles of Nrf3-Trim5 axis in vascular smooth muscle cell dysfunctions and neointimal hyperplasia.","authors":"Qishan Chen,Shasha Sun,Zhenning Shi,Leyu Wang,Yumeng Wang,Ancheng Zheng,Xiaolei Xu,Mei Yang,Kun Sun,Qingzhong Xiao,Li Zhang","doi":"10.1093/cvr/cvaf084","DOIUrl":"https://doi.org/10.1093/cvr/cvaf084","url":null,"abstract":"AIMSNeointimal hyperplasia (NIH) characterized by vascular smooth muscle cell (VSMC) dysfunctions plays a critical role in many vascular diseases including atherosclerosis and restenosis, which leads to serious ischemic complications and has limited therapeutic approaches. Our previous studies confirm a critical role for nuclear factor erythroid 2-related factor 3 (Nrf3) in VSMC differentiation. However, little is known about the functional implications of Nrf3 in NIH.METHODS AND RESULTSTranscriptome dataset and human atherosclerotic samples were used to determine Nrf3 expression levels. Global (Nrf3-/-) and VSMC-specific (Nrf3ΔSMC) Nrf3 knockout mice were used to assess the role of Nrf3 in VSMC function and injury-induced NIH. Complementary molecular methods were performed to identify Nrf3 downstream targets and elucidate the regulatory role of Nrf3 in target gene regulation. Porcine carotid stenting model was used to validate the therapeutic effects of Nrf3 inhibition in vascular remodeling.Transcriptomic data and immunostaining analysis showed increased levels of Nrf3, and a positive correlation between Nrf3 and NIH in the human atherosclerotic vessels. Various pathophysiological stimuli induced endoplasmic reticulum (ER) stress which enhanced Nrf3 expression via Activating Transcription Factor 4 (ATF4). Nrf3 overexpression promoted both human and mouse VSMC proliferation, migration, and inflammatory response, while opposite effects were observed when Nrf3 was deleted or knockdown. Nrf3-/- and Nrf3ΔSMC mice showed decreased VSMC accumulation and attenuated vascular injury-induced NIH. Mechanistically, tripartite motif-containing 5 (Trim5), a genetic risk locus for coronary artery disease, was identified as a functional downstream target of Nrf3 in VSMCs and in injured arteries. Nrf3 enhanced autophagy in VSMCs and injured arteries by upregulating Trim5 expression, which subsequently promoted dysfunctions of VSMCs, thereby increasing injury-induced NIH. Importantly, restoring either Nrf3 or Trim5 expression in Nrf3-/- mice rescued the arterial phenotypes observed in Nrf3-/- mice. Critically, the porcine carotid artery restenosis induced by ballooning and stenting was significantly reduced by suppressing Nrf3 expression through perivascular administration of the Nrf3 inhibitors.CONCLUSIONSWe comprehensively demonstrate that Nrf3 is a novel modulator in VSMC dysfunctions and injury-induced NIH. Nrf3 exerts its pathological functions by transcriptional activation of Trim5 gene, which in turn triggers autophagy in VSMCs and injured arteries, promoting arterial remodeling. Inhibiting the Nrf3-Trim5 signal axis ameliorates injury-induced NIH, offering novel therapeutics for treating patients with NIH-related vascular diseases.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"95 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144065569","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":"Deficiency of NPR-C triggers high salt-induced thoracic aortic dissection by impairing mitochondrial homeostasis.","authors":"Jin-Qiu Wei,Yi Yang,Wen-Hui Zhai,Jia-Jia Zhao,Yi-Hang Yang,Yuan-Yuan Kang,Qi-Fang Huang,Wei Zhang,Wu-Wei Rong,Qian-Wan Deng,Jing Chen,Xiao-Fei Ye,Ping-Jin Gao,Zhe Wang,Xiao-Dong Li,Ji-Guang Wang","doi":"10.1093/cvr/cvaf085","DOIUrl":"https://doi.org/10.1093/cvr/cvaf085","url":null,"abstract":"AIMSThoracic aortic dissection (TAD) is a highly fatal disease lacking effective pharmacologic interventions in clinical practice. Emerging evidence indicates that the natriuretic peptide receptor C (NPR-C) plays a crucial role in the regulation of cardiovascular diseases. However, the precise involvement of NPR-C in TAD remains elusive. In this study, the role and molecular mechanisms of NPR-C in the pathogenesis of TAD were investigated.METHODS AND RESULTSThrough integrated analyses of human TAD transcriptome and single-cell sequencing data sets, we identified that NPR-C was downregulated in the aortas of acute TAD patients and in beta-aminopropionitrile (BAPN)-treated mice. Intriguingly, vascular smooth muscle cell (VSMC)-specific NPR-C knockout (NPR-CSMKO) mice, rather than endothelial cell-specific NPR-C knockout mice, developed TAD after treated with angiotensin II (Ang II) plus high salt diet (HSD), but not Ang II alone. Loss of NPR-C function promoted extracellular matrix degeneration, VSMCs apoptosis and inflammation. RNA-sequencing analysis revealed that mitochondrial fatty acid oxidation (FAO) genes were significantly downregulated in the thoracic aortas of NPR-CSMKO mice treated with Ang II plus HSD. Notably, the expression of HADHB, a subunit of mitochondrial trifunctional protein (MTP) responsible for FAO, was obviously decreased in NPR-CSMKO mice treated with Ang II plus HSD. Mechanistically, knockdown of NPR-C activated ERK1/2 pathway, which decreased the expression and activity of peroxisome proliferator-activated receptor γ (PPARγ) and inhibited HADHB expression. Furthermore, NPR-C agonist, C-ANP4-23, mitigated the progression of TAD in BAPN-treated mice. Activation of MTP by spermidine (SPD) effectively prevented TAD formation in NPR-CSMKO mice treated with Ang II plus HSD.CONCLUSIONSOur data highlight a critical role of HSD in triggering TAD and a previously unrecognized role of NPR-C that protects against TAD through regulating mitochondrial homeostasis. Therefore, NPR-C activation and SPD supplementation could be new prevention and treatment strategies for TAD.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"42 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144065570","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 Beating Heart: art meets science in the story of the heart.","authors":"Robin P Choudhury","doi":"10.1093/cvr/cvaf054","DOIUrl":"https://doi.org/10.1093/cvr/cvaf054","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"35 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143945421","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":"Endothelial IGF-1 signaling: a conductor of vascular barrier function and LDL trafficking in atherogenesis.","authors":"Cong Liu,Joanna M Kalucka","doi":"10.1093/cvr/cvaf082","DOIUrl":"https://doi.org/10.1093/cvr/cvaf082","url":null,"abstract":"","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"52 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143945458","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":"Proteomic profiling reveals a higher presence of glycolytic enzymes in human atherosclerotic lesions with unfavourable histological characteristics","authors":"Kaylin C A Palm, Xiaoke Yin, Ferheen Baig, Konstantinos Theofilatos, Sander W van der Laan, Gert J de Borst, Dominique P V de Kleijn, Johann Wojta, Stefan Stojkovic, Manuel Mayr, Hester M den Ruijter, Gerard Pasterkamp, Ernest Diez Benavente, Michal Mokry","doi":"10.1093/cvr/cvaf077","DOIUrl":"https://doi.org/10.1093/cvr/cvaf077","url":null,"abstract":"Aims Molecular characterization of vulnerable atherosclerotic plaques often relies on transcriptomic data. However, RNA expression may not consistently align with protein expression. The proteomic landscape linked to plaque vulnerability is underexplored in human lesions. In this study, we analyzed a large mass spectrometry-based proteomics dataset from the plaque tissue of 320 patients to identify the molecular mechanisms associated with vulnerable plaques. Previous studies have shown significant differences in cell metabolism in murine atherosclerosis models, prompting an in-depth description of expression of key enzymes in glycolysis in human atherosclerotic plaques. Methods and results Atherosclerotic lesions from 320 patients undergoing carotid endarterectomy surgery were collected (200 discovery set and 120 for the validation set) and underwent proteomic analyses. Plaque samples were digested, enriched for extracellular matrix proteins, and processed for untargeted proteomics analysis. The resulting protein levels were linked to pathological plaque characteristics, bulk and single cell transcriptomics, and clinical data. Proteomic analysis of 200 human atherosclerotic carotid lesions detected 1499 proteins with most showing poor correlation with RNA levels. We identified 240 proteins associated with plaque vulnerability index (PVI) (FDR<0.05), including key glycolysis enzymes: HK3 (P=0.003, FDR=0.03), PKM (P=0.008, FDR=0.05), and LDHA (P=0.006, FDR=0.04). The observed associations were mainly driven by macrophage content and fat content, reflected the severity of pre-operative symptoms, exhibited significant sex differences, and correlated with plaque haemorrhage biomarker BLVRB. Validation in 120 patients confirmed HK3 and PKM's association with plaque progression and clinical symptoms (all P<0.001). Conclusion Enzymes involved in the glycolysis process are more abundant in plaques with vulnerable histological characteristics and are significantly associated with plaque hemorrhage biomarker BLVRB. This implies that plaque destabilization may be driven by higher glycolysis metabolism, which may contribute to plaque haemorrhage. This association was stronger in women, underlining the important role of energy metabolism in sex-specific mechanisms of atherosclerotic disease.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"31 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143940262","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":"Living myocardial slices: walking the path towards standardization","authors":"Jort S A van der Geest, Teun P de Boer, Cesare M Terracciano, Thomas Thum, Andreas Dendorfer, Pieter A Doevendans, Linda W van Laake, Joost P G Sluijter, Vasco Sampaio-Pinto","doi":"10.1093/cvr/cvaf079","DOIUrl":"https://doi.org/10.1093/cvr/cvaf079","url":null,"abstract":"Cardiovascular disease remains a persistent global health burden, underscoring the necessity for effective therapeutic strategies. Despite significant advances, the ability to mechanistically study human disease and predict clinical outcomes remains limited, especially in complex diseases such as heart failure. This limitation is evident through the continuous high attrition rates in drug development pipelines. To address these challenges and contribute to improved pre-clinical studies, there is a need for platforms that more accurately recapitulate the human heart. This need increased the interest in living myocardial slices (LMS) – thin sections of the heart of approximately 100-400 μm. LMS retain the native multicellular architecture of the heart and enable extended ex vivo culture. However, as their utilization grows, so does variability in preparation methodologies and readouts. This review provides an overview of differences in sample selection, interspecies variations, intra-cardiac differences, and potential confounding factors. Additionally, we examine culture methods, addressing electrical and mechanical stimulation differences, and medium compositions. Our review concludes by highlighting the current limitations of LMS research and offer guidelines for standardization and future applications. The ultimate aim of this review is to serve as a resource for researchers working with LMS and for those entering this field. By presenting the landscape of methodological considerations, we aim to facilitate informed decision-making in study design and execution. We advocate for accurate reporting of methodologies to promote reproducibility and comparability across studies, advancing LMS research and strengthening its role as a valuable addition to the current drug development toolbox and basic cardiovascular research.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"67 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143940263","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":"RNA interference versus antibody-based PCSK9 inhibition for the prevention of cardiovascular disease: A drug-target Mendelian randomization study","authors":"Eloi Gagnon, Dipender Gill, Jérôme Bourgault, Émilie Gobeil, Patricia L Mitchell, Arnaud Girard, Audrey Paulin, Christian Couture, Yohan Bossé, Sébastien Thériault, Patrick Mathieu, Marie-Claude Vohl, André Tchernof, Kausik K Ray, John J P Kastelein, Benoit J Arsenault","doi":"10.1093/cvr/cvaf078","DOIUrl":"https://doi.org/10.1093/cvr/cvaf078","url":null,"abstract":"Aims RNA interference therapies targeting liver expression of the gene proprotein convertase subtilisin/kexin type 9 (PCSK9) lower low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (apoB) levels. As opposed to monoclonal antibodies, which neutralise PCSK9 circulating protein, their effect on atherosclerotic cardiovascular disease (ASCVD) outcomes is unknown. We used genetic variants in the PCSK9 locus influencing PCSK9 function or gene expression in the liver to determine whether antibodies against PCSK9 and RNA interference therapies could have comparable effects on ASCVD. Methods and results We performed genome-wide genotyping and RNA sequencing of 504 human liver sample and identified a genetic variant (rs472495) explaining 5.6% of liver PCSK9 gene expression to mimic lifelong RNA interference of PCSK9. We used the PCSK9 R46L variant, known to alter PCSK9 function, to model antibody-based PCSK9 inhibition. For each standard deviation decrease in apoB levels, both variants were similarly associated with coronary artery disease risk: (OR = 0.40 [95% CI: 0.31-0.51], p = 3.7e-13 for rs472495 which affects liver PCSK9 expression) and (OR = 0.48 [95% CI: 0.43-0.55], p = 1.3e-28 for R46L which affects protein levels). Comparable effects of these two genetic inhibition approaches were observed for aortic stenosis, heart failure, ischemic stroke, type 2 diabetes and glycemic traits as well as non-alcoholic fatty liver disease and liver enzymes. Conclusions For a given reduction in apoB levels, genetically predicted reductions in PCSK9 function (mimicking PCSK9 neutralizing antibodies) and liver PCSK9 gene expression levels (mimicking PCSK9 RNA interference) were comparably associated with a lower risk of coronary artery disease. These genetic data suggest that LDL-C/apoB reductions may provide cardiovascular benefits, regardless of how PCSK9 function is inhibited.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"76 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143932466","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":"Atrial remodelling and atrial fibrillation self-sustaining: the role of circulating circDGCR8","authors":"Yuanfeng Gao, Ying Dong, Nan Jiang, Hanrui Zhang, Zheng Liu, Qianhui Wang, Yuan Fu, Jing Li, Zhiqing Li, Huize Pan, Xianing Zheng, Lingyu Zhan, Xinchun Yang, Li Xu, Mulei Chen","doi":"10.1093/cvr/cvaf060","DOIUrl":"https://doi.org/10.1093/cvr/cvaf060","url":null,"abstract":"Aims The prediction of atrial fibrillation (AF) progression and post-ablation recurrence is currently based on empirical estimates, leading to suboptimal predictive accuracy. This study investigates whether atrial remodelling, a key factor in the severity of atrial cardiomyopathy, could serve as a shared substrate influencing both AF progression and recurrence. We aimed to identify circular RNAs (circRNAs) associated with atrial remodelling and to evaluate their ability to predict AF progression and recurrence. Methods and results We assessed the differential expression of plasma circRNAs between paroxysmal (PAF) and persistent AF (PsAF) patients using microarray analysis. Selected candidate circRNAs were validated through qPCR following rigorous statistical and bioinformatics analysis. circDGCR8 was consistently found to be up-regulated in PsAF compared with PAF patients. Additionally, circDGCR8 was significantly up-regulated in human atrial fibroblasts treated with angiotensin II (AngII). Gain- and loss-of-function studies suggested that circDGCR8 could promote atrial remodelling at cellular level by enhancing collagen production and fibroblast proliferation. Overexpression of circDGCR8 in human cardiac fibroblasts significantly altered the gene expression spectrum, impacting pathways including IL-17 signalling and TNF signalling. Moreover, circDGCR8 levels were positively correlated with atrial fibrosis, as indicated by increased percentages of low voltage zones. The predictive value of circDGCR8 was evaluated in two cohorts: (i) PAF patients monitored for 36 months with progression to PsAF as the endpoint, and (ii) AF patients who underwent radiofrequency ablation followed for 12 months to assess recurrence. In both cohorts, higher level of circDGCR8 was associated with increased risks of AF progression and post-ablation recurrence. Conclusion Our results suggest that circDGCR8, associated with atrial remodelling, holds potential as a predictive biomarker for both AF progression and post-ablation recurrence.","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":"35 1","pages":""},"PeriodicalIF":10.8,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143920207","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":"Causal cardiovascular risk factors for dementia: insights from observational and genetic studies.","authors":"Emilie Westerlin Kjeldsen, Ruth Frikke-Schmidt","doi":"10.1093/cvr/cvae235","DOIUrl":"10.1093/cvr/cvae235","url":null,"abstract":"<p><p>The escalating prevalence of dementia worldwide necessitates preventive strategies to mitigate its extensive health, psychological, and social impacts. As the prevalence of dementia continues to rise, gaining insights into its risk factors and causes becomes paramount, given the absence of a definitive cure. Cardiovascular disease has emerged as a prominent player in the complex landscape of dementia. Preventing dyslipidaemia, unhealthy western-type diets, hypertension, diabetes, being overweight, physical inactivity, smoking, and high alcohol intake have the potential to diminish not only cardiovascular disease but also dementia. The purpose of this review is to present our current understanding of cardiovascular risk factors for Alzheimer's disease and vascular dementia (VaD) by using clinical human data from observational, genetic studies and clinical trials, while elaborating on potential mechanisms. Hypertension and Type 2 diabetes surface as significant causal risk factors for both Alzheimer's disease and VaD, as consistently illustrated in observational and Mendelian randomization studies. Anti-hypertensive drugs and physical activity have been shown to improve cognitive function in clinical trials. Important to note is that robust genome-wide association studies are lacking for VaD, and indeed more and prolonged clinical trials are needed to establish these findings and investigate other risk factors. Trials should strategically target individuals at the highest dementia risk, identified using risk charts incorporating genetic markers, biomarkers, and cardiovascular risk factors. Understanding causal risk factors for dementia will optimize preventive measures, and the implementation of well-known therapeutics can halt or alleviate dementia symptoms if started early. Needless to mention is that future health policies should prioritize primordial prevention from early childhood to prevent risk factors from even occurring in the first place. Together, understanding the role of cardiovascular risk factors in dementia, improving genome-wide association studies for VaD, and advancing clinical trials are crucial steps in addressing this significant public health challenge.</p>","PeriodicalId":9638,"journal":{"name":"Cardiovascular Research","volume":" ","pages":"537-549"},"PeriodicalIF":10.2,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12054631/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}