Arteriosclerosis, Thrombosis, and Vascular Biology最新文献

{"title":"Regulation of Collecting Lymphatic Vessel Contractile Function by TRPV4 Channels.","authors":"Mary E Schulz, Victoria L Akerstrom, Kejing Song, Sarah E Broyhill, Min Li, Michelle D Lambert, Tatia B Goldberg, Raghu P Kataru, Jinyeon Shin, Stephen E Braun, Charles E Norton, Rafael S Czepielewski, Babak J Mehrara, Timothy L Domeier, Scott D Zawieja, Jorge A Castorena-Gonzalez","doi":"10.1161/ATVBAHA.124.322100","DOIUrl":"10.1161/ATVBAHA.124.322100","url":null,"abstract":"<p><strong>Background: </strong>Dysregulation of TRPV4 (transient receptor potential vanilloid type 4)-mediated signaling has been associated with inflammation and tissue fibrosis, both of which are key features in the pathophysiology of lymphatic system diseases; however, the expression and functional roles of lymphatic TRPV4 channels remain largely unexplored.</p><p><strong>Methods: </strong>We generated a single-cell RNA sequencing dataset from microdissected mouse collecting lymphatic vessels to characterize the expression of <i>Trpv4</i>. Using a novel <i>Trpv4</i>^<i>fx/fx</i> mouse strain and the Cre-lines <i>Prox1</i>-CreER^<i>T2</i> and <i>LysM</i>-Cre we assessed the role of TRPV4 channels in lymphatic endothelial cells and peri-lymphatic myeloid cells, respectively. Confocal microscopy and extensive functional experimentation on isolated and pressurized lymphatics, including measurements of intracellular calcium activity, were used to validate our single-cell RNA sequencing findings and to elucidate the underlying mechanisms. Clinical significance was assessed using biopsies from patients with breast cancer-related lymphedema.</p><p><strong>Results: </strong>We characterized the single-cell transcriptome of collecting lymphatic vessels and surrounding tissues. <i>Trpv4</i> was highly enriched in lymphatic endothelial cells and in a subset of <i>Lyve1</i>+ (lymphatic vessel endothelial hyaluronan receptor 1) macrophages displaying a tissue-resident profile. In clinical samples, breast cancer-related lymphedema was associated with increased infiltration of macrophages coexpressing LYVE1 and TRPV4. Pharmacological activation of TRPV4 channels led to contractile dysregulation in isolated collecting lymphatics. The response was multiphasic, including initial vasospasm and subsequent vasodilation and inhibition of contractions, which was associated with the activation of TXA2Rs (thromboxane A2 receptors) in lymphatic muscle cells by secreted prostanoids from TRPV4+ myeloid cells, and increased nitric oxide (and perhaps other vasodilatory prostanoids) from lymphatic endothelial cells. The TXA2R-mediated vasospasm resulted from increased mobilization of calcium from intracellular stores through inositol trisphosphate receptors and store-operated calcium entry.</p><p><strong>Conclusions: </strong>Our results uncovered a novel mechanism of lymphatic contractile dysregulation mediated by the crosstalk between TRPV4-expressing myeloid cells, including LYVE1+ macrophages, and lymphatic muscle cells or lymphatic endothelial cells. These findings highlight potentially important roles of TRPV4 channels in lymphatic dysfunction associated with inflammation, including secondary lymphedema.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"e412-e436"},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12266246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075600","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}

{"title":"Alcohol, Liver Disease, and Peripheral Arterial Disease: Epidemiology, Mechanisms, and Clinical Implications.","authors":"Shuai Yuan, Scott M Damrauer, Susanna C Larsson","doi":"10.1161/ATVBAHA.125.322136","DOIUrl":"10.1161/ATVBAHA.125.322136","url":null,"abstract":"<p><p>Peripheral arterial disease (PAD) is a major vascular complication associated with significant morbidity and mortality. While traditional cardiovascular risk factors such as smoking, hypertension, and diabetes are well established, emerging evidence suggests that alcohol consumption, alcoholic liver disease, and metabolic-associated steatotic liver disease may also contribute to PAD risk. This review synthesizes current epidemiological evidence linking alcohol intake, alcoholic liver disease, and metabolic-associated steatotic liver disease to PAD and explores potential mechanisms, including atherosclerosis, endothelial dysfunction, chronic inflammation, dyslipidemia, and coagulation abnormalities. Observational studies suggest a possible protective effect of light-to-moderate alcohol consumption though genetic studies challenge this notion. In addition, alcoholic liver disease and metabolic-associated steatotic liver disease are increasingly recognized as contributors to systemic vascular dysfunction and PAD progression. In conclusion, given the rising burden of liver disease, it is crucial to determine whether PAD screening is warranted in patients with high-risk alcoholic liver disease and metabolic-associated steatotic liver disease. Addressing modifiable risk factors and optimizing pharmacological interventions may help mitigate PAD risk. Future research should focus on longitudinal studies, sex- and ethnicity-specific differences, and omics-based approaches to refine risk prediction, early detection, and targeted interventions.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1493-1504"},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274114","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}

{"title":"Role of Clot Formation and Plasminogen Activation in Lower Urinary Tract Pathologies.","authors":"Jonathan J Molina, Ana Lidia Flores-Mireles","doi":"10.1161/ATVBAHA.125.321600","DOIUrl":"10.1161/ATVBAHA.125.321600","url":null,"abstract":"<p><p>Hemostasis, a critical physiological process, is essential for stopping bleeding and initiating tissue repair after injury. It involves a tightly coordinated interplay between coagulation (blood clotting) and fibrinolysis (clot breakdown). Dysregulation of hemostasis can result in a wide range of diseases, such as infections, cancers, metabolic disorders, and neurodegenerative disorders. In the urinary tract, disruption of homeostasis and induction of hemostasis by diseases or foreign bodies (such as urinary catheters) can lead to various problems, such as infections, inflammation, and structural damage. Furthermore, hemostatic proteins have been associated with severe cancer progression. Thus, highlighting the roles of clot formation and plasminogen activation in urinary tract pathologies is important. This review details the pathogenesis of the urinary tract and urothelial carcinoma, as well as the roles of clot formation and plasminogen activation during disease onset and progression.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1471-1478"},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12321223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144752193","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}

{"title":"Correction to: Endothelial-Specific Expression of Mitochondrial Thioredoxin Promotes Ischemia-Mediated Arteriogenesis and Angiogenesis.","authors":"Shengchuan Dai, Yun He, Haifeng Zhang, Luyang Yu, Ting Wan, Zhe Xu, Dennis Jones, Hong Chen, Wang Min","doi":"10.1161/ATV.0000000000000189","DOIUrl":"https://doi.org/10.1161/ATV.0000000000000189","url":null,"abstract":"","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":"45 9","pages":"e467"},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144940412","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":"Factor XI and Heart Failure.","authors":"David Gailani","doi":"10.1161/ATVBAHA.125.323395","DOIUrl":"10.1161/ATVBAHA.125.323395","url":null,"abstract":"","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1670-1671"},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793348","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":"Lats1/2 Are Essential for Developmental Vascular Remodeling and Biomechanical Adaptation to Shear Stress.","authors":"Mitzy A Cowdin, Tuli Pramanik, Shelby R Mohr-Allen, Yuting Fu, Austin Mills, Stephen B Spurgin, Victor D Varner, George E Davis, Ondine Cleaver","doi":"10.1161/ATVBAHA.124.322258","DOIUrl":"10.1161/ATVBAHA.124.322258","url":null,"abstract":"<p><strong>Background: </strong>Mechanical cues exerted by shear stress from blood flow remodel an initial vascular plexus into a ramifying array of large and small vessels. Hemodynamic forces trigger changes in endothelial cell (EC) gene expression and dynamic alterations in cell shape and adhesion. The objective of this study is to elucidate the role of the Lats (large tumor suppressor) 1 and Lats2 (Lats1/2) Hippo pathway kinases in EC transducing of hemodynamic signals as vessels form.</p><p><strong>Methods: </strong>Lats1/2 were genetically deleted in murine ECs (<i>Lats</i>^{<i>iECDKO</i>}) and developing vessels were evaluated using immunofluorescence. Primary human pulmonary artery ECs were used to model endothelial response to blood flow and Lats1/2 depletion was achieved via siRNA treatment. EC junctions, cytoskeletal rearrangements, cell shape, and polarization were assessed using immunofluorescence. mRNA expression analyses and Western blotting were performed to understand changes in the response of cultured ECs to shear stress.</p><p><strong>Results: </strong>We report a critical requirement for Lats1/2 in adapting to blood flow during vascular development. When Lats1/2 are genetically deleted in ECs, embryos develop severe defects in blood vessel formation, which lead to embryonic lethality by embryonic day 11.5. Vessel patterning and circulation initiate properly; however, remodeling of the initial vascular plexus fails due to lumen collapse. Lats1/2 depletion in cultured ECs leads to failed polarization, elongation, and VEcad (vascular endothelial cadherin 5 or Cdh5) junctional maturation under flow. Finally, YAP (Yes-associated protein)/TAZ (transcriptional coactivator with PDZ-binding motif) codepletion in Lats1/2 depleted conditions leads to a partial rescue of phenotypes in vivo and in vitro.</p><p><strong>Conclusions: </strong>Our results suggest that Lats1/2 deficient cells no longer respond to laminar shear stress, in vivo and in vitro. This work identifies Lats1 and Lats2 as critical transducers of biomechanical cues during early blood vessel remodeling. This study provides new targets for treating vascular diseases and new directions for efforts to generate vascularized tissues for replacement therapies.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1521-1542"},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274118","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":"METTL3 Exacerbates Intimal Hyperplasia by Facilitating m⁶A-YTHDC1-Dependent SGK1 Gene Transcription.","authors":"Jiaqi Huang, Qianqian Feng, Zhigang Dong, Zhuofan Li, Yihan Liu, Ran Xu, Zhujiang Liu, Qianhui Ding, Xueyuan Yang, Fang Yu, Yiting Jia, Yuan Zhou, Wei Kong, Hao Tang, Yi Fu","doi":"10.1161/ATVBAHA.125.322961","DOIUrl":"10.1161/ATVBAHA.125.322961","url":null,"abstract":"<p><strong>Background: </strong>Vascular smooth muscle cell (VSMC) migration and proliferation substantially contribute to neointimal hyperplasia related to in-stent restenosis. N⁶-methyladenosine (m⁶A) modification catalyzed by the METTL3 (methyltransferase-like 3)-containing methyltransferase complex is the most abundant RNA epigenetic modification in eukaryotes, but the role of m⁶A RNA methylation in VSMC migration and proliferation and neointima formation remains highly controversial.</p><p><strong>Methods: </strong>Primary human and rat VSMCs were utilized for in vitro experiments. VSMC-specific METTL3 knockout mice (<i>Mettl3</i>^flox/flox<i>Myh11</i>-CreER^T2) were generated to explore the role of METTL3 in carotid artery wire injury in vivo. Methylated RNA immunoprecipitation sequencing was performed to screen for genes targeted for METTL3-catalyzed m⁶A RNA methylation. Methylation site mapping, methylated RNA immunoprecipitation-quantitative polymerase chain reaction, chromatin immunoprecipitation-quantitative polymerase chain reaction, and reporter gene assays were used to explore how METTL3 modulates target gene expression.</p><p><strong>Results: </strong>METTL3 expression was consistently upregulated in the neointima of mice subjected to carotid wire injury and in those of patients who underwent carotid endarterectomy. VSMC-specific METTL3 deficiency significantly attenuated neointima formation in mouse carotid arteries after wire injury. Accordingly, METTL3 ablation markedly repressed VSMC proliferation both in vitro and in vivo. Mechanistically, METTL3 directly catalyzed the m⁶A methylation of SGK1 (serum/glucocorticoid-regulated kinase 1) mRNA and subsequently facilitated its transcription, a process that was dependent on the established association between the SGK1 transcript and SGK1 promoter DNA via recruitment of the m⁶A reader YTHDC1 (YT521-B homology domain-containing protein 1). Conversely, SGK1 overexpression abolished the METTL3 deficiency-mediated suppression of VSMC proliferation and postinjury neointima formation.</p><p><strong>Conclusions: </strong>METTL3-catalyzed m⁶A RNA methylation promoted VSMC proliferation and exacerbated postinjury neointima formation by facilitating YTHDC1-dependent SGK1 gene transcription. Targeting the METTL3-YTHDC1-SGK1 axis to modulate VSMC proliferation may be a potential strategy for in-stent restenosis therapy.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"e437-e453"},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144551817","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":"Plasminogen Activation in Oral Mucosal Immunopathology.","authors":"Lina C Fellah, Lakmali M Silva","doi":"10.1161/ATVBAHA.125.322733","DOIUrl":"10.1161/ATVBAHA.125.322733","url":null,"abstract":"<p><p>The Plg (plasminogen)/Pln (plasmin) system plays a broad range of roles in maintaining homeostasis at the oral mucosa, including homeostatic inflammation, tissue remodeling, and wound healing. Deregulation of these processes can lead to either increased or decreased proteolytic activity of Pln and, thereby, oral mucosal immunopathology. Here, we present a basic overview of the PAS (Plg activation system) components in the oral cavity and discuss how these factors are involved in oral mucosal homeostasis and disease pathogenesis. We reason that the role of the Plg/Pln system becomes evident in individuals with the Mendelian genetic defect, congenital Plg deficiency, who are predisposed to severe periodontitis in childhood due to defective fibrinolysis. Consistent with Plg deficiency as a risk factor for periodontitis, recent discovery of significant association between genetic polymorphisms in <i>PLG</i> and periodontal disease suggests <i>PLG</i> variants as candidate risk indicators for common forms of periodontitis.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1479-1487"},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144752192","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":"Tricuspid Aortic Valve Regurgitation Associates With Ascending Aortic Aneurysm Through Endothelial Activation and Lipoprotein Infiltration.","authors":"David Freiholtz, Claudia Reyes-Goya, Karin Lång, Otto Bergman, Christian Olsson, Malin Granbom Koski, Michael Dismorr, Cecilia Österholm, Kenneth Caidahl, Anders Franco-Cereceda, Per Eriksson, Anton Gisterå, Hanna M Björck","doi":"10.1161/ATVBAHA.125.323112","DOIUrl":"10.1161/ATVBAHA.125.323112","url":null,"abstract":"<p><strong>Background: </strong>An abnormal accumulation of immune cells and inflammation has been described in ascending aortic aneurysm, but the factor driving disease initiation remains elusive. Interestingly, ascending aortic dilatation often occurs alongside aortic regurgitation but rarely with aortic stenosis. We sought to investigate ascending aortic aneurysm initiation by assessing the relation between aortic regurgitation and vascular activation and inflammation.</p><p><strong>Methods: </strong>In this prospective cohort study, patients with tricuspid aortic valves undergoing elective open-heart surgery were included. Aortic specimens from organ donors were obtained through the University of Miami Tissue Bank. Spatial transcriptomics measured gene expression in nondilated aortic endothelium, intima, and subintima. Immunohistochemistry determined protein expression. Aortic dimensions were recorded preoperatively and 10 years after surgery using echocardiography. Aortic gene expression affected by physiological blood flow was previously measured in Wistar rats.</p><p><strong>Results: </strong>We show a mesenchymal activation of endothelial cells, possibly mediated by bidirectional flow, in the nondilated ascending aorta of patients with aortic regurgitation, accompanied by intimal infiltration, retention, and oxidation of apoB-containing lipoproteins. We further observed intimal upregulation of genes coding for core proteins of lipoprotein-binding proteoglycans and the <i>OLR1</i> (oxidized low-density lipoprotein receptor 1), the latter by infiltrating macrophages and in association with progressive inflammation and dilatation. None of the above was observed in patients with aortic stenosis. Notably, surgical replacement of regurgitant valves, but not stenotic valves, mitigated 10-year aortic growth.</p><p><strong>Conclusions: </strong>Our results highlight a distinct pathological role of aortic regurgitation in ascending aortic aneurysm formation by promoting mesenchymal activation of endothelial cells and lipoprotein-related immune cell infiltration and inflammation in patients with tricuspid aortic valves. We also provide novel insights into the long-term impact of surgical aortic valve replacement on ascending aortic growth and suggest a diagnostic or therapeutic target in oxidized low-density lipoprotein cholesterol.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1636-1647"},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12379797/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144752194","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}

{"title":"Nontraditional Risk Factors for Peripheral Artery Disease: Setting the Scene.","authors":"Matthew A Allison, Janet T Powell, Jonathan Golledge","doi":"10.1161/ATVBAHA.125.323193","DOIUrl":"10.1161/ATVBAHA.125.323193","url":null,"abstract":"<p><p>Atherothrombotic occlusion and narrowing of the arteries supplying blood to the legs, usually referred to as peripheral artery disease, affects 6% of adults and is associated with impaired quality of life and increased risk of major adverse events including death. Peripheral artery disease has been relatively understudied and has not been subject to the same scrutiny and investigation that characterizes coronary artery disease. Importantly, there are subtle differences between peripheral and coronary artery disease with respect to traditional risk factors, and there may be marked differences in nontraditional risk factors. Here, we provide a brief description of the population burden, pathophysiology, and traditional risk factors for peripheral artery disease, which is intended as the introduction to a series of reviews focusing on nontraditional risk factors for this disorder. We highlight the planned reviews in the series and how these may act as an important impetus to address the unmet need of improving outcomes in people with peripheral artery disease.</p>","PeriodicalId":8401,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology","volume":" ","pages":"1488-1492"},"PeriodicalIF":7.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793351","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}