Angiogenesis最新文献

Circulating endothelial cells: a key biomarker of persistent fatigue after hospitalization for COVID-19

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-12-20 DOI: 10.1007/s10456-024-09959-z

David M. Smadja, Sven Günther, Pauline Cavagna, Bertrand Renaud, Dominique Salmon, Bertrand Hermann, Brigitte Ranque, Cédric Lemogne, Jean-Luc Diehl, Aurélien Philippe

引用次数: 0

Neuropilin-1 controls vascular permeability through juxtacrine regulation of endothelial adherens junctions

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-12-12 DOI: 10.1007/s10456-024-09963-3

Sagnik Pal, Yangyang Su, Emmanuel Nwadozi, Lena Claesson-Welsh, Mark Richards

{"title":"Neuropilin-1 controls vascular permeability through juxtacrine regulation of endothelial adherens junctions","authors":"Sagnik Pal, Yangyang Su, Emmanuel Nwadozi, Lena Claesson-Welsh, Mark Richards","doi":"10.1007/s10456-024-09963-3","DOIUrl":"10.1007/s10456-024-09963-3","url":null,"abstract":"<div><p>Neuropilin-1 (NRP1) regulates endothelial cell (EC) biology through modulation of vascular endothelial growth factor receptor 2 (VEGFR2) signalling by presenting VEGFA to VEGFR2. How NRP1 impacts VEGFA-mediated vascular hyperpermeability has however remained unresolved, described as exerting either a positive or a passive function. Using EC-specific <i>Nrp1</i> knock-out mice, we discover that EC-expressed NRP1 exerts an organotypic role. In the ear skin, VEGFA/VEGFR2-mediated vascular leakage was increased following loss of EC NRP1, implicating NRP1 in negative regulation of VEGFR2 signalling. In contrast, in the back skin and trachea, loss of EC NRP1 decreased vascular leakage. In accordance, phosphorylation of vascular endothelial (VE)-cadherin was increased in the ear skin but suppressed in the back skin of <i>Nrp1</i> iECKO mice. NRP1 expressed on perivascular cells has been shown to impact VEGF-mediated VEGFR2 signalling. Importantly, expression of NRP1 on perivascular cells was more abundant in the ear skin than in the back skin. Global loss of NRP1 resulted in suppressed VEGFA-induced vascular leakage in the ear skin, implicating perivascular NRP1 as a juxtacrine co-receptor of VEGFA in this compartment. Altogether, we demonstrate that perivascular NRP1 is an active participant in EC VEGFA/VEGFR2 signalling and acts as an organotypic modifier of EC biology.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 1","pages":""},"PeriodicalIF":9.2,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-024-09963-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142810976","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}

引用次数: 0

Genetic and pharmacological targeting of mTORC1 in mouse models of arteriovenous malformation expose non-cell autonomous signalling in HHT

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-12-11 DOI: 10.1007/s10456-024-09961-5

Antonio Queiro-Palou, Yi Jin, Lars Jakobsson

{"title":"Genetic and pharmacological targeting of mTORC1 in mouse models of arteriovenous malformation expose non-cell autonomous signalling in HHT","authors":"Antonio Queiro-Palou, Yi Jin, Lars Jakobsson","doi":"10.1007/s10456-024-09961-5","DOIUrl":"10.1007/s10456-024-09961-5","url":null,"abstract":"<div><p>Arteriovenous malformations (AVMs) are abnormal high flow shunts between arteries and veins with major negative impact on the cardiovascular system. Inherited loss-of-function (LOF) mutations in endoglin, encoding an endothelial cell (EC) expressed co-receptor for BMP9/10, causes the disease HHT1/Osler-Weber-Rendu, characterized by bleeding and AVMs. Here we observe increased activity of the downstream signalling complex mTORC1 within the retinal vasculature of HHT mouse models. To investigate its importance in AVM biology, concerning subvascular action, cell specificity, signalling strength and kinetics we combine timed genetic and antibody-based models of HHT with genetic mTORC1 inhibition or activation through EC specific deletion of <i>Rptor</i> or <i>Tsc1</i>. Results demonstrate that EC mTORC1 activation is secondary to endoglin LOF and mainly a consequence of systemic effects following AVM. While genetic EC inhibition of mTORC1 only showed tendencies towards reduced AVM severity, EC overactivation counterintuitively reduced it, implying that mTORC1 must be within a certain range to facilitate AVM. Complete inhibition of mTORC1 signalling by rapamycin provided the strongest therapeutic effect, pointing to potential involvement of RAPTOR-independent pathways or AVM-promoting effects of non-ECs in this pathology.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 1","pages":""},"PeriodicalIF":9.2,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-024-09961-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806051","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}

引用次数: 0

Alk1/Endoglin signaling restricts vein cell size increases in response to hemodynamic cues

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-12-10 DOI: 10.1007/s10456-024-09955-3

Zeenat Diwan, Jia Kang, Emma Tsztoo, Arndt F. Siekmann

{"title":"Alk1/Endoglin signaling restricts vein cell size increases in response to hemodynamic cues","authors":"Zeenat Diwan, Jia Kang, Emma Tsztoo, Arndt F. Siekmann","doi":"10.1007/s10456-024-09955-3","DOIUrl":"10.1007/s10456-024-09955-3","url":null,"abstract":"<div><p>Hemodynamic cues are thought to control blood vessel hierarchy through a shear stress set point, where flow increases lead to blood vessel diameter expansion, while decreases in blood flow cause blood vessel narrowing. Aberrations in blood vessel diameter control can cause congenital arteriovenous malformations (AVMs). We show in zebrafish embryos that while arteries behave according to the shear stress set point model, veins do not. This behavior is dependent on distinct arterial and venous endothelial cell (EC) shapes and sizes. We show that arterial ECs enlarge more strongly when experiencing higher flow, as compared to vein cells. Through the generation of chimeric embryos, we discover that this behavior of vein cells depends on the bone morphogenetic protein (BMP) pathway components Endoglin and Alk1. <i>Endoglin</i> (<i>eng</i>) or <i>alk1</i> (<i>acvrl1</i>) mutant vein cells enlarge when in normal hemodynamic environments, while we do not observe a phenotype in either <i>acvrl1</i> or <i>eng</i> mutant ECs in arteries. We further show that an increase in vein diameters initiates AVMs in <i>eng</i> mutants, secondarily leading to higher flow to arteries. These enlarge in response to higher flow through increasing arterial EC sizes, fueling the AVM. This study thus reveals a mechanism through which BMP signaling limits vein EC size increases in response to flow and provides a framework for our understanding of how a small number of mutant vein cells via flow-mediated secondary effects on wildtype arterial ECs can precipitate larger AVMs in disease conditions, such as hereditary hemorrhagic telangiectasia (HHT).</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 1","pages":""},"PeriodicalIF":9.2,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-024-09955-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142798365","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}

引用次数: 0

Inhibition of Angiopoietin-2 rescues sporadic brain arteriovenous malformations by reducing pericyte loss

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-12-05 DOI: 10.1007/s10456-024-09957-1

Tianqi Tu, Shikun Zhang, Jingwei Li, Chendan Jiang, Jian Ren, Shiju Zhang, Xiaosheng Meng, Hao Peng, Dong Xing, Hongqi Zhang, Tao Hong, Jiaxing Yu

{"title":"Inhibition of Angiopoietin-2 rescues sporadic brain arteriovenous malformations by reducing pericyte loss","authors":"Tianqi Tu, Shikun Zhang, Jingwei Li, Chendan Jiang, Jian Ren, Shiju Zhang, Xiaosheng Meng, Hao Peng, Dong Xing, Hongqi Zhang, Tao Hong, Jiaxing Yu","doi":"10.1007/s10456-024-09957-1","DOIUrl":"10.1007/s10456-024-09957-1","url":null,"abstract":"<div><p>Brain arteriovenous malformations (bAVMs) are a major cause of hemorrhagic stroke in children and young adults. These lesions are thought to result from somatic <i>KRAS/BRAF</i> mutations in brain endothelial cells (bECs). In this study, we introduce a new bAVM model by inducing a brain endothelial-specific <i>Braf</i><sup>V600E</sup> mutation using the <i>Slc1o1c1</i>(BAC)-CreER driver line. The pathological characteristics of this model resemble human bAVMs, including dilated and hyperpermeable vessels, as well as parenchymal hemorrhage. We observed that these lesions showed a typical reduction in pericyte coverage and disruption of the pericyte-endothelial cell connection. Additionally, we found that ANGPT2 levels were significantly increased in the endothelium of bAVM lesions, which may be a critical factor in the pericyte deficits of the malformed vessels. Treatment with an ANGPT2 neutralizing antibody confirmed that blocking ANGPT2 can restore pericyte density in bAVM lesions, improve pericyte coverage around microvessels, enhance tight junction protein coverage related to endothelial cells, and normalize endothelial barrier function. In summary, our findings suggest that increased ANGPT2 expression in endothelial cells with the <i>Braf</i><sup>V600E</sup> mutation is a key factor in pericyte deficiencies in bAVMs, highlighting the potential effectiveness of anti-ANGPT2 therapy in treating bAVMs.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 1","pages":""},"PeriodicalIF":9.2,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142778469","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}

引用次数: 0

Extracellular nicotinamide phosphoribosyltransferase (eNAMPT) drives abnormal pericyte-rich vasculature in triple-negative breast cancer

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-12-05 DOI: 10.1007/s10456-024-09956-2

Marianna Moro, Federica Carolina Balestrero, Giorgia Colombo, Simone Torretta, Nausicaa Clemente, Valerio Ciccone, Erika Del Grosso, Sandra Donnini, Cristina Travelli, Fabrizio Condorelli, Sabina Sangaletti, Armando A. Genazzani, Ambra A. Grolla

{"title":"Extracellular nicotinamide phosphoribosyltransferase (eNAMPT) drives abnormal pericyte-rich vasculature in triple-negative breast cancer","authors":"Marianna Moro, Federica Carolina Balestrero, Giorgia Colombo, Simone Torretta, Nausicaa Clemente, Valerio Ciccone, Erika Del Grosso, Sandra Donnini, Cristina Travelli, Fabrizio Condorelli, Sabina Sangaletti, Armando A. Genazzani, Ambra A. Grolla","doi":"10.1007/s10456-024-09956-2","DOIUrl":"10.1007/s10456-024-09956-2","url":null,"abstract":"<div><p>Tumour angiogenesis supports malignant cells with oxygen and nutrients to promote invasion and metastasis. A number of cytokines released in situ participate in the recruitment of endothelial cells and pericytes to trigger the formation of novel blood vessels, which are often abnormal, leaky, and disorganized. Nicotinamide phosphoribosyltransferase is a key intracellular enzyme involved in NAD metabolism and is up regulated in many cancers to meet bioenergetic demands. Yet, the same protein is also secreted extracellularly (eNAMPT), where it acts as a pro-inflammatory cytokine. High plasma eNAMPT levels have been reported in breast cancer patients and correlate with aggressiveness and prognosis. We now report that in a triple-negative breast cancer model, enriching the tumour microenvironment with eNAMPT leads to abundant angiogenesis and increased metastatization. Atypically, the eNAMPT-mediated pro-angiogenic effect is mainly directed to NG2<sup>+</sup> pericytes. Indeed, eNAMPT acts as chemoattractant for pericytes and coordinates vessel-like tube formation, in synergism with the classical factor PDGF-BB. Stimulation of pericytes by eNAMPT leads to a pro-inflammatory activation, characterized by the overexpression of key chemokines (CXCL8, CXCL1, CCL2) and VCAM1, via NF-κB signalling. All these effects were ablated by the use of C269, an anti-eNAMPT neutralizing antibody, suggesting that this might represent a novel anti-angiogenic pharmacological approach for triple-negative breast cancer. </p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 1","pages":""},"PeriodicalIF":9.2,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142778468","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}

引用次数: 0

Study on mitogenic activity of serum from patients with total coronary occlusions: relation to duration of occlusion

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-12-02 DOI: 10.1007/s10456-024-09958-0

V. Tchaikovski, G. S. Werner, M. Fritzenwanger, E. Jandt, Johannes Waltenberger

{"title":"Study on mitogenic activity of serum from patients with total coronary occlusions: relation to duration of occlusion","authors":"V. Tchaikovski, G. S. Werner, M. Fritzenwanger, E. Jandt, Johannes Waltenberger","doi":"10.1007/s10456-024-09958-0","DOIUrl":"10.1007/s10456-024-09958-0","url":null,"abstract":"<div><p>In contrast to the extensive evidence from animal studies, only few human data are available on the relation of vascular growth factors and collateral function as well as on the conditions which may modify their release or function. In 31 patients with total coronary occlusion (TCOs) blood was collected from distal to the occlusion site (collateral circulation) and from the aortic root (systemic circulation). Serum was used to assess its mitogenic potential in [<sup>3</sup>H]-thymidine incorporation assay on human umbilical vein endothelial cells. Serum from patients with the duration of occlusion between 1 and 3 months was significantly more mitogenic as compared to either shorter or longer duration of occlusion. None of the demographic or clinical factors correlated with the mitogenic activity of serum. Serum from patients with TCOs shows a particular time-dependent mitogenic profile with a maximal activity between 1 and 3 months following the occlusion. This profile corresponds to the experimentally described time-line of strongest collateral development and indicates the time-window for possible modification.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 1","pages":""},"PeriodicalIF":9.2,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-024-09958-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142757973","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}

引用次数: 0

Retinal pigment epithelial cells reduce vascular leak and proliferation in retinal neovessels 视网膜色素上皮细胞可减少视网膜新生血管的血管渗漏和增殖。

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-11-27 DOI: 10.1007/s10456-024-09954-4

Simone Tzaridis, Edith Aguilar, Michael I. Dorrell, Martin Friedlander, Kevin T. Eade

{"title":"Retinal pigment epithelial cells reduce vascular leak and proliferation in retinal neovessels","authors":"Simone Tzaridis, Edith Aguilar, Michael I. Dorrell, Martin Friedlander, Kevin T. Eade","doi":"10.1007/s10456-024-09954-4","DOIUrl":"10.1007/s10456-024-09954-4","url":null,"abstract":"<div><p>In multiple neurodegenerative diseases, including age-related macular degeneration, retinitis pigmentosa, and macular telangiectasia type 2 (MacTel), retinal pigment epithelial (RPE)-cells proliferate and migrate into the neuroretina, forming intraretinal pigment plaques. Though these pigmentary changes are hallmarks of disease progression, it is unknown if their presence is protective or detrimental.</p><p>Here, we first evaluated the impact of pigment plaques on vascular changes and disease progression in MacTel. In a retrospective, longitudinal study, we analyzed multimodal retinal images of patients with MacTel and showed that pigment plaques were associated with decreased vascular leakage and stabilized neovascular growth. We then modeled the underlying pathomechanisms of pigment plaque formation in aberrant neovascular growth using the very-low-density lipoprotein receptor mutant (<i>Vldlr</i><sup>−/−</sup>) mouse. Our data indicated that during RPE-proliferation, migration and accumulation along neovessels RPE-cells underwent epithelial-mesenchymal transition (EMT). Pharmacologic inhibition of EMT in <i>Vldlr</i><sup>−/−</sup> mice decreased pigment coverage, and exacerbated neovascular growth and vascular leakage.</p><p>Our findings indicate that the proliferation, migration and perivascular accumulation of RPE-cells stabilize vascular proliferation and exudation, thereby exerting a protective effect on the diseased retina. We conclude that interfering with this “natural repair mechanism” may have detrimental effects on the course of the disease and should thus be avoided.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 1","pages":""},"PeriodicalIF":9.2,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-024-09954-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142724782","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}

引用次数: 0

Correction: Mitochondrial control of hypoxia-induced pathological retinal angiogenesis 更正：线粒体控制缺氧诱导的病理性视网膜血管生成。

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-10-19 DOI: 10.1007/s10456-024-09952-6

Hitomi Yagi, Myriam Boeck, Shen Nian, Katherine Neilsen, Chaomei Wang, Jeff Lee, Yan Zeng, Matthew Grumbine, Ian R. Sweet, Taku Kasai, Kazuno Negishi, Sasha A. Singh, Masanori Aikawa, Ann Hellström, Lois E. H. Smith, Zhongjie Fu

引用次数: 0

Angiogenesis is limited by LIC1-mediated lysosomal trafficking 血管生成受到 LIC1 介导的溶酶体贩运的限制。

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-10-02 DOI: 10.1007/s10456-024-09951-7

Dymonn Johnson, Sarah Colijn, Jahmiera Richee, Joseph Yano, Margaret Burns, Andrew E. Davis, Van N. Pham, Amra Saric, Akansha Jain, Ying Yin, Daniel Castranova, Mariana Melani, Misato Fujita, Stephanie Grainger, Juan S. Bonifacino, Brant M. Weinstein, Amber N. Stratman

{"title":"Angiogenesis is limited by LIC1-mediated lysosomal trafficking","authors":"Dymonn Johnson, Sarah Colijn, Jahmiera Richee, Joseph Yano, Margaret Burns, Andrew E. Davis, Van N. Pham, Amra Saric, Akansha Jain, Ying Yin, Daniel Castranova, Mariana Melani, Misato Fujita, Stephanie Grainger, Juan S. Bonifacino, Brant M. Weinstein, Amber N. Stratman","doi":"10.1007/s10456-024-09951-7","DOIUrl":"10.1007/s10456-024-09951-7","url":null,"abstract":"<div><p>Dynein cytoplasmic 1 light intermediate chain 1 (LIC1, <i>DYNC1LI1</i>) is a core subunit of the dynein motor complex. The LIC1 subunit also interacts with various cargo adaptors to regulate Rab-mediated endosomal recycling and lysosomal degradation. Defects in this gene are predicted to alter dynein motor function, Rab binding capabilities, and cytoplasmic cargo trafficking. Here, we have identified a <i>dync1li1</i> zebrafish mutant, harboring a premature stop codon at the exon 12/13 splice acceptor site, that displays increased angiogenesis. In vitro, LIC1-deficient human endothelial cells display increases in cell surface levels of the pro-angiogenic receptor VEGFR2, SRC phosphorylation, and Rab11-mediated endosomal recycling. In vivo, endothelial-specific expression of constitutively active <i>Rab11a</i> leads to excessive angiogenesis, similar to the <i>dync1li1</i> mutants. Increased angiogenesis is also evident in zebrafish harboring mutations in <i>rilpl1/2</i>, the adaptor proteins that promote Rab docking to Lic1 to mediate lysosomal targeting. These findings suggest that LIC1 and the Rab-adaptor proteins RILPL1 and 2 restrict angiogenesis by promoting degradation of VEGFR2-containing recycling endosomes. Disruption of LIC1- and RILPL1/2-mediated lysosomal targeting increases Rab11-mediated recycling endosome activity, promoting excessive SRC signaling and angiogenesis.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 4","pages":"943 - 962"},"PeriodicalIF":9.2,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142360950","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}

引用次数: 0