Angiogenesis最新文献

{"title":"Human atherosclerotic plaque transcriptomics reveals endothelial beta-2 spectrin as a potential regulator a leaky plaque microvasculature phenotype","authors":"Timo Rademakers,&nbsp;Marco Manca,&nbsp;Han Jin,&nbsp;Tanguy Orban,&nbsp;Ljubica Matic Perisic,&nbsp;Hubertus J. M. Frissen,&nbsp;Frank Rühle,&nbsp;Petra Hautvast,&nbsp;Jos van Rijssel,&nbsp;Kim van Kuijk,&nbsp;Barend M. E. Mees,&nbsp;Carine J. Peutz-Kootstra,&nbsp;Sylvia Heeneman,&nbsp;Mat J. A. P. Daemen,&nbsp;Gerard Pasterkamp,&nbsp;Monika Stoll,&nbsp;Marc A. M. J. van Zandvoort,&nbsp;Ulf Hedin,&nbsp;Franck Dequiedt,&nbsp;Jaap D. van Buul,&nbsp;Judith C. Sluimer,&nbsp;Erik A. L. Biessen","doi":"10.1007/s10456-024-09921-z","DOIUrl":"10.1007/s10456-024-09921-z","url":null,"abstract":"<div><p>The presence of atherosclerotic plaque vessels is a critical factor in plaque destabilization. This may be attributable to the leaky phenotype of these microvessels, although direct proof for this notion is lacking. In this study, we investigated molecular and cellular patterns of stable and hemorrhaged human plaque to identify novel drivers of intraplaque vessel dysfunction. From transcriptome data of a human atherosclerotic lesion cohort, we reconstructed a co-expression network, identifying a gene module strongly and selectively correlated with both plaque microvascular density and inflammation. Spectrin Beta Non-Erythrocytic 1 (<i>sptbn1</i>) was identified as one of the central hubs of this module (along with <i>zeb1</i> and <i>dock1</i>) and was selected for further study based on its predominant endothelial expression. Silencing of <i>sptbn1</i> enhanced leukocyte transmigration and vascular permeability in vitro, characterized by an increased number of focal adhesions and reduced junctional VE-cadherin. In vivo, <i>sptbn1</i> knockdown in zebrafish impaired the development of the caudal vein plexus. Mechanistically, increased substrate stiffness was associated with <i>sptbn1</i> downregulation in endothelial cells in vitro and in human vessels. Plaque SPTBN1 mRNA and protein expression were found to correlate with an enhanced presence of intraplaque hemorrhage and future cardiovascular disease (CVD) events during follow-up. In conclusion, we identify SPTBN1 as a central hub gene in a gene program correlating with plaque vascularisation. SPTBN1 was regulated by substrate stiffness in vitro while silencing blocked vascular development in vivo, and compromised barrier function in vitro. Together, SPTBN1 is identified as a new potential regulator of the leaky phenotype of atherosclerotic plaque microvessels.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 3","pages":"461 - 474"},"PeriodicalIF":9.2,"publicationDate":"2024-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141080492","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":"Generation and characterisation of scalable and stable human pluripotent stem cell-derived microvascular-like endothelial cells for cardiac applications","authors":"Qasim A. Majid,&nbsp;Bishwa R. Ghimire,&nbsp;Bela Merkely,&nbsp;Anna M. Randi,&nbsp;Sian E. Harding,&nbsp;Virpi Talman,&nbsp;Gábor Földes","doi":"10.1007/s10456-024-09929-5","DOIUrl":"10.1007/s10456-024-09929-5","url":null,"abstract":"<div><p>Coronary microvascular disease (CMD) and its progression towards major adverse coronary events pose a significant health challenge. Accurate in vitro investigation of CMD requires a robust cell model that faithfully represents the cells within the cardiac microvasculature. Human pluripotent stem cell-derived endothelial cells (hPSC-ECs) offer great potential; however, they are traditionally derived via differentiation protocols that are not readily scalable and are not specified towards the microvasculature. Here, we report the development and comprehensive characterisation of a scalable 3D protocol enabling the generation of phenotypically stable cardiac hPSC-microvascular-like ECs (hPSC-CMVECs) and cardiac pericyte-like cells. These were derived by growing vascular organoids within 3D stirred tank bioreactors and subjecting the emerging 3D hPSC-ECs to high-concentration VEGF-A treatment (3DV). Not only did this promote phenotypic stability of the 3DV hPSC-ECs; single cell-RNA sequencing (scRNA-seq) revealed the pronounced expression of cardiac endothelial- and microvascular-associated genes. Further, the generated mural cells attained from the vascular organoid exhibited markers characteristic of cardiac pericytes. Thus, we present a suitable cell model for investigating the cardiac microvasculature as well as the endothelial-dependent and -independent mechanisms of CMD. Moreover, owing to their phenotypic stability, cardiac specificity, and high angiogenic potential, the cells described within would also be well suited for cardiac tissue engineering applications.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 3","pages":"561 - 582"},"PeriodicalIF":9.2,"publicationDate":"2024-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303486/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141074609","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":"Human iPSC and CRISPR targeted gene knock-in strategy for studying the somatic TIE2L914F mutation in endothelial cells","authors":"Bojana Lazovic,&nbsp;Hoang-Tuan Nguyen,&nbsp;Mohammadhassan Ansarizadeh,&nbsp;Leif Wigge,&nbsp;Franziska Kohl,&nbsp;Songyuan Li,&nbsp;Miguel Carracedo,&nbsp;Jere Kettunen,&nbsp;Luc Krimpenfort,&nbsp;Ramy Elgendy,&nbsp;Kati Richter,&nbsp;Laknee De Silva,&nbsp;Bilada Bilican,&nbsp;Prateek Singh,&nbsp;Pratik Saxena,&nbsp;Lars Jakobsson,&nbsp;Xuechong Hong,&nbsp;Lauri Eklund,&nbsp;Ryan Hicks","doi":"10.1007/s10456-024-09925-9","DOIUrl":"10.1007/s10456-024-09925-9","url":null,"abstract":"<div><p>Induced pluripotent stem cell (iPSC) derived endothelial cells (iECs) have emerged as a promising tool for studying vascular biology and providing a platform for modelling various vascular diseases, including those with genetic origins. Currently, primary ECs are the main source for disease modelling in this field. However, they are difficult to edit and have a limited lifespan. To study the effects of targeted mutations on an endogenous level, we generated and characterized an iPSC derived model for venous malformations (VMs). CRISPR-Cas9 technology was used to generate a novel human iPSC line with an amino acid substitution L914F in the TIE2 receptor, known to cause VMs. This enabled us to study the differential effects of VM causative mutations in iECs in multiple in vitro models and assess their ability to form vessels in vivo. The analysis of TIE2 expression levels in TIE2^L914F iECs showed a significantly lower expression of TIE2 on mRNA and protein level, which has not been observed before due to a lack of models with endogenous edited TIE2^L914F and sparse patient data. Interestingly, the TIE2 pathway was still significantly upregulated and TIE2 showed high levels of phosphorylation. TIE2^L914F iECs exhibited dysregulated angiogenesis markers and upregulated migration capability, while proliferation was not affected. Under shear stress TIE2^L914F iECs showed reduced alignment in the flow direction and a larger cell area than TIE2^WT iECs. In summary, we developed a novel TIE2^L914F iPSC-derived iEC model and characterized it in multiple in vitro models. The model can be used in future work for drug screening for novel treatments for VMs.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 3","pages":"523 - 542"},"PeriodicalIF":9.2,"publicationDate":"2024-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303492/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141069657","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":"CCL4 contributes to aging related angiogenic insufficiency through activating oxidative stress and endothelial inflammation","authors":"Ting-Ting Chang,&nbsp;Liang-Yu Lin,&nbsp;Ching Chen,&nbsp;Jaw-Wen Chen","doi":"10.1007/s10456-024-09922-y","DOIUrl":"10.1007/s10456-024-09922-y","url":null,"abstract":"<div><p>Aging is a natural process associated with chronic inflammation in the development of vascular dysfunction. We hypothesized that chemokine C-C motif ligands 4 (CCL4) might play a vital role in aging-related vascular dysfunction. Circulating CCL4 was up-regulated in elderly subjects and in aged animals. CCL4 inhibition reduced generation of reactive oxygen species (ROS), attenuated inflammation, and restored cell functions in endothelial progenitor cells from elderly subjects and in aged human aortic endothelial cells. CCL4 promoted cell aging, with impaired cell functioning, by activating ROS production and inflammation. CCL4 knockout mice and therapeutic administration of anti-CCL4 neutralizing antibodies exhibited vascular and dermal anti-aging effects, with improved wound healing, via the down-regulation of inflammatory proteins and the activation of angiogenic proteins. Altogether, our findings suggested that CCL4 may contribute to aging-related vascular dysfunction via activating oxidative stress and endothelial inflammation. CCL4 may be a potential therapeutic target for vascular protections during aging.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 3","pages":"475 - 499"},"PeriodicalIF":9.2,"publicationDate":"2024-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303582/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140910872","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":"Distinct roles of SOX9 in self-renewal of progenitors and mesenchymal transition of the endothelium","authors":"Jilai Zhao,&nbsp;Laura Sormani,&nbsp;Sebastien Jacquelin,&nbsp;Haiming Li,&nbsp;Cassandra Styke,&nbsp;Chenhao Zhou,&nbsp;Jonathan Beesley,&nbsp;Linus Oon,&nbsp;Simranpreet Kaur,&nbsp;Seen-Ling Sim,&nbsp;Ho Yi Wong,&nbsp;James Dight,&nbsp;Ghazaleh Hashemi,&nbsp;Abbas Shafiee,&nbsp;Edwige Roy,&nbsp;Jatin Patel,&nbsp;Kiarash Khosrotehrani","doi":"10.1007/s10456-024-09927-7","DOIUrl":"10.1007/s10456-024-09927-7","url":null,"abstract":"<div><p>Regenerative capabilities of the endothelium rely on vessel-resident progenitors termed endothelial colony forming cells (ECFCs). This study aimed to investigate if these progenitors are impacted by conditions (i.e., obesity or atherosclerosis) characterized by increased serum levels of oxidized low-density lipoprotein (oxLDL), a known inducer of Endothelial-to-Mesenchymal Transition (EndMT). Our investigation focused on understanding the effects of EndMT on the self-renewal capabilities of progenitors and the associated molecular alterations. In the presence of oxLDL, ECFCs displayed classical features of EndMT, through reduced endothelial gene and protein expression, function as well as increased mesenchymal genes, contractility, and motility. Additionally, ECFCs displayed a dramatic loss in self-renewal capacity in the presence of oxLDL. RNA-sequencing analysis of ECFCs exposed to oxLDL validated gene expression changes suggesting EndMT and identified SOX9 as one of the highly differentially expressed genes. ATAC sequencing analysis identified SOX9 binding sites associated with regions of dynamic chromosome accessibility resulting from oxLDL exposure, further pointing to its importance. EndMT phenotype and gene expression changes induced by oxLDL in vitro or high fat diet (HFD) in vivo were reversed by the silencing of SOX9 in ECFCs or the endothelial-specific conditional knockout of Sox9 in murine models. Overall, our findings support that EndMT affects vessel-resident endothelial progenitor’s self-renewal. SOX9 activation is an early transcriptional event that drives the mesenchymal transition of endothelial progenitor cells. The identification of the molecular network driving EndMT in vessel-resident endothelial progenitors presents a new avenue in understanding and preventing a range of condition where this process is involved.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 3","pages":"545 - 560"},"PeriodicalIF":9.2,"publicationDate":"2024-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303482/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140908369","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":"Blood flow regulates acvrl1 transcription via ligand-dependent Alk1 activity","authors":"Anthony R. Anzell,&nbsp;Amy B. Kunz,&nbsp;James P. Donovan,&nbsp;Thanhlong G. Tran,&nbsp;Xinyan Lu,&nbsp;Sarah Young,&nbsp;Beth L. Roman","doi":"10.1007/s10456-024-09924-w","DOIUrl":"10.1007/s10456-024-09924-w","url":null,"abstract":"<div><p>Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant disease characterized by the development of arteriovenous malformations (AVMs) that can result in significant morbidity and mortality. HHT is caused primarily by mutations in bone morphogenetic protein receptors <i>ACVRL1</i>/ALK1, a signaling receptor, or endoglin (<i>ENG</i>), an accessory receptor. Because overexpression of <i>Acvrl1</i> prevents AVM development in both <i>Acvrl1</i> and <i>Eng</i> null mice, enhancing <i>ACVRL1</i> expression may be a promising approach to development of targeted therapies for HHT. Therefore, we sought to understand the molecular mechanism of <i>ACVRL1</i> regulation. We previously demonstrated in zebrafish embryos that <i>acvrl1</i> is predominantly expressed in arterial endothelial cells and that expression requires blood flow. Here, we document that flow dependence exhibits regional heterogeneity and that <i>acvrl1</i> expression is rapidly restored after reinitiation of flow. Furthermore, we find that <i>acvrl1</i> expression is significantly decreased in mutants that lack the circulating Alk1 ligand, Bmp10, and that, in the absence of flow, intravascular injection of BMP10 or the related ligand, BMP9, restores <i>acvrl1</i> expression in an Alk1-dependent manner. Using a transgenic <i>acvrl1:egfp</i> reporter line, we find that flow and Bmp10 regulate <i>acvrl1</i> at the level of transcription. Finally, we observe similar ALK1 ligand-dependent increases in <i>ACVRL1</i> in human endothelial cells subjected to shear stress. These data suggest that ligand-dependent Alk1 activity acts downstream of blood flow to maintain or enhance <i>acvrl1</i> expression via a positive feedback mechanism, and that ALK1 activating therapeutics may have dual functionality by increasing both ALK1 signaling flux and <i>ACVRL1</i> expression.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 3","pages":"501 - 522"},"PeriodicalIF":9.2,"publicationDate":"2024-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140896872","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":"IC100, a humanized therapeutic monoclonal anti-ASC antibody alleviates oxygen-induced retinopathy in mice","authors":"Huijun Yuan,&nbsp;Shaoyi Chen,&nbsp;Matthew R. Duncan,&nbsp;Juan Pablo de Rivero Vaccari,&nbsp;Robert W. Keane,&nbsp;W. Dalton Dietrich,&nbsp;Tsung-Han Chou,&nbsp;Merline Benny,&nbsp;Augusto F. Schmidt,&nbsp;Karen Young,&nbsp;Kevin K. Park,&nbsp;Vittorio Porciatti,&nbsp;M. Elizabeth Hartnett,&nbsp;Shu Wu","doi":"10.1007/s10456-024-09917-9","DOIUrl":"10.1007/s10456-024-09917-9","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;p&gt;Retinopathy of prematurity (ROP), which often presents with bronchopulmonary dysplasia (BPD), is among the most common morbidities affecting extremely premature infants and is a leading cause of severe vision impairment in children worldwide. Activations of the inflammasome cascade and microglia have been implicated in playing a role in the development of both ROP and BPD. Apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) is pivotal in inflammasome assembly. Utilizing mouse models of both oxygen-induced retinopathy (OIR) and BPD, this study was designed to test the hypothesis that hyperoxia induces ASC speck formation, which leads to microglial activation and retinopathy, and that inhibition of ASC speck formation by a humanized monoclonal antibody, IC100, directed against ASC, will ameliorate microglial activation and abnormal retinal vascular formation.&lt;/p&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;p&gt;We first tested ASC speck formation in the retina of ASC-citrine reporter mice expressing ASC fusion protein with a C-terminal citrine (fluorescent GFP isoform) using a BPD model that causes both lung and eye injury by exposing newborn mice to room air (RA) or 85% O&lt;sub&gt;2&lt;/sub&gt; from postnatal day (P) 1 to P14. The retinas were dissected on P14 and retinal flat mounts were used to detect vascular endothelium with AF-594-conjugated isolectin B4 (IB4) and citrine-tagged ASC specks. To assess the effects of IC100 on an OIR model, newborn ASC citrine reporter mice and wildtype mice (C57BL/6 J) were exposed to RA from P1 to P6, then 75% O&lt;sub&gt;2&lt;/sub&gt; from P7 to P11, and then to RA from P12 to P18. At P12 mice were randomized to the following groups: RA with placebo PBS (RA-PBS), O&lt;sub&gt;2&lt;/sub&gt; with PBS (O&lt;sub&gt;2&lt;/sub&gt;-PBS), O&lt;sub&gt;2&lt;/sub&gt; + IC100 intravitreal injection (O&lt;sub&gt;2&lt;/sub&gt;-IC100-IVT), and O&lt;sub&gt;2&lt;/sub&gt; + IC100 intraperitoneal injection (O&lt;sub&gt;2&lt;/sub&gt;-IC100-IP). Retinal vascularization was evaluated by flat mount staining with IB4. Microglial activation was detected by immunofluorescence staining for allograft inflammatory factor 1 (AIF-1) and CD206. Retinal structure was analyzed on H&amp;E-stained sections, and function was analyzed by pattern electroretinography (PERG). RNA-sequencing (RNA-seq) of the retinas was performed to determine the transcriptional effects of IC100 treatment in OIR.&lt;/p&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;p&gt;ASC specks were significantly increased in the retinas by hyperoxia exposure and colocalized with the abnormal vasculature in both BPD and OIR models, and this was associated with increased microglial activation. Treatment with IC100-IVT or IC100-IP significantly reduced vaso-obliteration and intravitreal neovascularization. IC100-IVT treatment also reduced retinal microglial activation, restored retinal structure, and improved retinal function. RNA-seq showed that IC100 treatment corrected the induction of genes associated with angiogenesis, leukocyte migration, and VEGF signaling caused by O&lt;sub&gt;2&lt;/","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 3","pages":"423 - 440"},"PeriodicalIF":9.2,"publicationDate":"2024-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140856165","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":"Somatic BrafV600E mutation in the cerebral endothelium induces brain arteriovenous malformations","authors":"Tianqi Tu,&nbsp;Jiaxing Yu,&nbsp;Chendan Jiang,&nbsp;Shikun Zhang,&nbsp;Jingwei Li,&nbsp;Jian Ren,&nbsp;Shiju Zhang,&nbsp;Yuan Zhou,&nbsp;Ziwei Cui,&nbsp;Haohan Lu,&nbsp;Xiaosheng Meng,&nbsp;Zhanjing Wang,&nbsp;Dong Xing,&nbsp;Hongqi Zhang,&nbsp;Tao Hong","doi":"10.1007/s10456-024-09918-8","DOIUrl":"10.1007/s10456-024-09918-8","url":null,"abstract":"<div><p>Current treatments of brain arteriovenous malformation (BAVM) are associated with considerable risks and at times incomplete efficacy. Therefore, a clinically consistent animal model of BAVM is urgently needed to investigate its underlying biological mechanisms and develop innovative treatment strategies. Notably, existing mouse models have limited utility due to heterogenous and untypical phenotypes of AVM lesions. Here we developed a novel mouse model of sporadic BAVM that is consistent with clinical manifestations in humans. Mice with <i>Braf</i>^V600E mutations in brain ECs developed BAVM closely resembled that of human lesions. This strategy successfully induced BAVMs in mice across different age groups and within various brain regions. Pathological features of BAVM were primarily dilated blood vessels with reduced vascular wall stability, accompanied by spontaneous hemorrhage and neuroinflammation. Single-cell sequencing revealed differentially expressed genes that were related to the cytoskeleton, cell motility, and intercellular junctions. Early administration of Dabrafenib was found to be effective in slowing the progression of BAVMs; however, its efficacy in treating established BAVM lesions remained uncertain. Taken together, our proposed approach successfully induced BAVM that closely resembled human BAVM lesions in mice, rendering the model suitable for investigating the pathogenesis of BAVM and assessing potential therapeutic strategies.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 3","pages":"441 - 460"},"PeriodicalIF":9.2,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140849011","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":"Correction: Granzyme B degrades extracellular matrix and promotes inflammation and choroidal neovascularization","authors":"Gideon Obasanmi,&nbsp;Manjosh Uppal,&nbsp;Jing Z. Cui,&nbsp;Jeanne Xi,&nbsp;Myeong Jin Ju,&nbsp;Jun Song,&nbsp;Eleanor To,&nbsp;Siqi Li,&nbsp;Wania Khan,&nbsp;Darian Cheng,&nbsp;John Zhu,&nbsp;Lyden Irani,&nbsp;Isa Samad,&nbsp;Julie Zhu,&nbsp;Hyung-Suk Yoo,&nbsp;Alexandre Aubert,&nbsp;Jonathan Stoddard,&nbsp;Martha Neuringer,&nbsp;David J. Granville,&nbsp;Joanne A. Matsubara","doi":"10.1007/s10456-024-09919-7","DOIUrl":"10.1007/s10456-024-09919-7","url":null,"abstract":"","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 3","pages":"375 - 377"},"PeriodicalIF":9.2,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303458/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140854145","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":"Systemic glucocorticoids use in post-COVID-syndrome patients does not affect retinal microcirculation","authors":"T. Kuchler,&nbsp;C. Schmaderer","doi":"10.1007/s10456-024-09926-8","DOIUrl":"10.1007/s10456-024-09926-8","url":null,"abstract":"","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 3","pages":"287 - 291"},"PeriodicalIF":9.2,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140854146","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}