Angiogenesis最新文献_第10页

Systemic glucocorticoids link to long-term microvascular injury in COVID-19 全身糖皮质激素与 COVID-19 的长期微血管损伤有关。

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-04-24 DOI: 10.1007/s10456-024-09923-x

Qian Yang, Cai Yun Xia, Ying Cai, Yan Fang Zhang, Dao Ting Li, Shu Qi Wu, Peng Hu

引用次数: 0

Interleukin-6 drives endothelial glycocalyx damage in COVID-19 and bacterial sepsis 白细胞介素-6 在 COVID-19 和细菌性败血症中驱动内皮糖萼损伤

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-04-10 DOI: 10.1007/s10456-024-09916-w

Carolin Christina Drost, Alexandros Rovas, Irina Osiaevi, Klaus Schughart, Alexander Lukasz, Wolfgang A. Linke, Hermann Pavenstädt, Philipp Kümpers

{"title":"Interleukin-6 drives endothelial glycocalyx damage in COVID-19 and bacterial sepsis","authors":"Carolin Christina Drost, Alexandros Rovas, Irina Osiaevi, Klaus Schughart, Alexander Lukasz, Wolfgang A. Linke, Hermann Pavenstädt, Philipp Kümpers","doi":"10.1007/s10456-024-09916-w","DOIUrl":"10.1007/s10456-024-09916-w","url":null,"abstract":"<div><p>Damage of the endothelial glycocalyx (eGC) plays a central role in the development of vascular hyperpermeability and organ damage during systemic inflammation. However, the specific signalling pathways for eGC damage remain poorly defined. Aim of this study was to combine sublingual video-microscopy, plasma proteomics and live cell imaging to uncover further pathways of eGC damage in patients with coronavirus disease 2019 (COVID-19) or bacterial sepsis. This secondary analysis of the prospective multicenter MICROCODE study included 22 patients with COVID-19 and 43 patients with bacterial sepsis admitted to intermediate or intensive care units and 10 healthy controls. Interleukin-6 (IL-6) was strongly associated with damaged eGC and correlated both with eGC dimensions (r<sub>s</sub>=0.36, <i>p</i> = 0.0015) and circulating eGC biomarkers. In vitro, IL-6 reduced eGC height and coverage, which was inhibited by blocking IL-6 signalling with the anti-IL-6 receptor antibody tocilizumab or the Janus kinase inhibitor tofacitinib. Exposure of endothelial cells to 5% serum from COVID-19 or sepsis patients resulted in a significant decrease in eGC height, which was attenuated by co-incubation with tocilizumab. In an external COVID-19 cohort of 219 patients from Massachusetts General Hospital, a previously identified proteomic eGC signature correlated with IL-6 (r<sub>s</sub>=-0.58, <i>p</i> < 0.0001) and predicted the combined endpoint of 28-day mortality and/or intubation (ROC-AUC: 0.86 [95% CI: 0.81–0.91], <i>p</i> < 0.001). The data suggest that IL-6 may significantly drive eGC damage in COVID-19 and bacterial sepsis. Our findings provide valuable insights into pathomechanisms of vascular dysfunction during systemic inflammation and highlight the need for further in vivo studies.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 3","pages":"411 - 422"},"PeriodicalIF":9.2,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-024-09916-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140580247","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

Navigating tumor angiogenesis: therapeutic perspectives and myeloid cell regulation mechanism 肿瘤血管生成导航：治疗视角与髓细胞调控机制

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-04-06 DOI: 10.1007/s10456-024-09913-z

Fan Yang, Gloria Lee, Yi Fan

引用次数: 0

The role of vasculature and angiogenesis in respiratory diseases 血管和血管生成在呼吸系统疾病中的作用

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-04-05 DOI: 10.1007/s10456-024-09910-2

Maximilian Ackermann, Christopher Werlein, Edith Plucinski, Sophie Leypold, Mark P. Kühnel, Stijn E. Verleden, Hassan A. Khalil, Florian Länger, Tobias Welte, Steven J. Mentzer, Danny D. Jonigk

{"title":"The role of vasculature and angiogenesis in respiratory diseases","authors":"Maximilian Ackermann, Christopher Werlein, Edith Plucinski, Sophie Leypold, Mark P. Kühnel, Stijn E. Verleden, Hassan A. Khalil, Florian Länger, Tobias Welte, Steven J. Mentzer, Danny D. Jonigk","doi":"10.1007/s10456-024-09910-2","DOIUrl":"10.1007/s10456-024-09910-2","url":null,"abstract":"<div><p>In European countries, nearly 10% of all hospital admissions are related to respiratory diseases, mainly chronic life-threatening diseases such as COPD, pulmonary hypertension, IPF or lung cancer. The contribution of blood vessels and angiogenesis to lung regeneration, remodeling and disease progression has been increasingly appreciated. The vascular supply of the lung shows the peculiarity of dual perfusion of the pulmonary circulation (vasa publica), which maintains a functional blood-gas barrier, and the bronchial circulation (vasa privata), which reveals a profiled capacity for angiogenesis (namely intussusceptive and sprouting angiogenesis) and alveolar-vascular remodeling by the recruitment of endothelial precursor cells. The aim of this review is to outline the importance of vascular remodeling and angiogenesis in a variety of non-neoplastic and neoplastic acute and chronic respiratory diseases such as lung infection, COPD, lung fibrosis, pulmonary hypertension and lung cancer.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 3","pages":"293 - 310"},"PeriodicalIF":9.2,"publicationDate":"2024-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-024-09910-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140579701","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

Microglia in retinal angiogenesis and diabetic retinopathy 视网膜血管生成和糖尿病视网膜病变中的小胶质细胞。

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-04-02 DOI: 10.1007/s10456-024-09911-1

Aiyan Hu, Mirko H. H. Schmidt, Nora Heinig

{"title":"Microglia in retinal angiogenesis and diabetic retinopathy","authors":"Aiyan Hu, Mirko H. H. Schmidt, Nora Heinig","doi":"10.1007/s10456-024-09911-1","DOIUrl":"10.1007/s10456-024-09911-1","url":null,"abstract":"<div><p>Diabetic retinopathy has a high probability of causing visual impairment or blindness throughout the disease progression and is characterized by the growth of new blood vessels in the retina at an advanced, proliferative stage. Microglia are a resident immune population in the central nervous system, known to play a crucial role in regulating retinal angiogenesis in both physiological and pathological conditions, including diabetic retinopathy. Physiologically, they are located close to blood vessels and are essential for forming new blood vessels (neovascularization). In diabetic retinopathy, microglia become widely activated, showing a distinct polarization phenotype that leads to their accumulation around neovascular tufts. These activated microglia induce pathogenic angiogenesis through the secretion of various angiogenic factors and by regulating the status of endothelial cells. Interestingly, some subtypes of microglia simultaneously promote the regression of neovascularization tufts and normal angiogenesis in neovascularization lesions. Modulating the state of microglial activation to ameliorate neovascularization thus appears as a promising potential therapeutic approach for managing diabetic retinopathy.</p><h3>Graphical abstract</h3>\u0000<div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 3","pages":"311 - 331"},"PeriodicalIF":9.2,"publicationDate":"2024-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303477/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140334444","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

Vascular mimicry in zebrafish fin regeneration: how macrophages build new blood vessels 斑马鱼鳍再生中的血管模拟：巨噬细胞如何构建新血管

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-03-28 DOI: 10.1007/s10456-024-09914-y

Anita Senk, Jennifer Fazzari, Valentin Djonov

{"title":"Vascular mimicry in zebrafish fin regeneration: how macrophages build new blood vessels","authors":"Anita Senk, Jennifer Fazzari, Valentin Djonov","doi":"10.1007/s10456-024-09914-y","DOIUrl":"10.1007/s10456-024-09914-y","url":null,"abstract":"<div><p>Vascular mimicry has been thoroughly investigated in tumor angiogenesis. In this study, we demonstrate for the first time that a process closely resembling tumor vascular mimicry is present during physiological blood vessel formation in tissue regeneration using the zebrafish fin regeneration assay. At the fin-regenerating front, vasculature is formed by mosaic blood vessels with endothelial-like cells possessing the morphological phenotype of a macrophage and co-expressing both endothelial and macrophage markers within single cells. Our data demonstrate that the vascular segments of the regenerating tissue expand, in part, through the transformation of adjacent macrophages into endothelial-like cells, forming functional, perfused channels and contributing to the de novo formation of microvasculature. Inhibiting the formation of tubular vascular-like structures by CVM-1118 prevents vascular mimicry and network formation resulting in a 70% shorter regeneration area with 60% reduced vessel growth and a complete absence of any signs of regeneration in half of the fin area. Additionally, this is associated with a significant reduction in macrophages. Furthermore, depleting macrophages using macrophage inhibitor PLX-3397, results in impaired tissue regeneration and blood vessel formation, namely a reduction in the regeneration area and vessel network by 75% in comparison to controls.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 3","pages":"397 - 410"},"PeriodicalIF":9.2,"publicationDate":"2024-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303510/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140317713","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

Connective tissue disorders in COVID-19: Reply to “People with a connective tissue disorder may be especially vulnerable to the endothelial damage that characterizes long COVID due to the fragility of their vasculature and slow wound healing” COVID-19 中的结缔组织疾病：对 "结缔组织疾病患者由于血管脆弱和伤口愈合缓慢，可能特别容易受到长 COVID 所特有的内皮损伤 "的答复。

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-03-26 DOI: 10.1007/s10456-024-09915-x

Xiaoming Wu, Valerie A. Novakovic, Jialan Shi

引用次数: 0

Granzyme B degrades extracellular matrix and promotes inflammation and choroidal neovascularization 颗粒酶 B 降解细胞外基质，促进炎症和脉络膜新生血管形成

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-03-18 DOI: 10.1007/s10456-024-09909-9

Gideon Obasanmi, Manjosh Uppal, Jing Z. Cui, Jeanne Xi, Myeong Jin Ju, Jun Song, Eleanor To, Siqi Li, Wania Khan, Darian Cheng, John Zhu, Lyden Irani, Isa Samad, Julie Zhu, Hyung-Suk Yoo, Alexandre Aubert, Jonathan Stoddard, Martha Neuringer, David J. Granville, Joanne A. Matsubara

{"title":"Granzyme B degrades extracellular matrix and promotes inflammation and choroidal neovascularization","authors":"Gideon Obasanmi, Manjosh Uppal, Jing Z. Cui, Jeanne Xi, Myeong Jin Ju, Jun Song, Eleanor To, Siqi Li, Wania Khan, Darian Cheng, John Zhu, Lyden Irani, Isa Samad, Julie Zhu, Hyung-Suk Yoo, Alexandre Aubert, Jonathan Stoddard, Martha Neuringer, David J. Granville, Joanne A. Matsubara","doi":"10.1007/s10456-024-09909-9","DOIUrl":"10.1007/s10456-024-09909-9","url":null,"abstract":"<div><p>Age-related macular degeneration (AMD) is a common retinal neurodegenerative disease among the elderly. Neovascular AMD (nAMD), a leading cause of AMD-related blindness, involves choroidal neovascularization (CNV), which can be suppressed by anti-angiogenic treatments. However, current CNV treatments do not work in all nAMD patients. Here we investigate a novel target for AMD. Granzyme B (GzmB) is a serine protease that promotes aging, chronic inflammation and vascular permeability through the degradation of the extracellular matrix (ECM) and tight junctions. Extracellular GzmB is increased in retina pigment epithelium (RPE) and mast cells in the choroid of the healthy aging outer retina. It is further increased in donor eyes exhibiting features of nAMD and CNV. Here, we show in RPE-choroidal explant cultures that exogenous GzmB degrades the RPE-choroid ECM, promotes retinal/choroidal inflammation and angiogenesis while diminishing anti-angiogenic factor, thrombospondin-1 (TSP-1). The pharmacological inhibition of either GzmB or mast-cell degranulation significantly reduces choroidal angiogenesis. In line with our in vitro data, GzmB-deficiency reduces the extent of laser-induced CNV lesions and the age-related deterioration of electroretinogram (ERG) responses in mice. These findings suggest that targeting GzmB, a serine protease with no known endogenous inhibitors, may be a potential novel therapeutic approach to suppress CNV in nAMD.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 3","pages":"351 - 373"},"PeriodicalIF":9.2,"publicationDate":"2024-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-024-09909-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140146628","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

Photoreceptors inhibit pathological retinal angiogenesis through transcriptional regulation of Adam17 via c-Fos 光感受器通过 c-Fos 对 Adam17 进行转录调控，从而抑制病理性视网膜血管生成。

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-03-14 DOI: 10.1007/s10456-024-09912-0

Xudong Wang, Tianxi Wang, Satoshi Kaneko, Emil Kriukov, Enton Lam, Manon Szczepan, Jasmine Chen, Austin Gregg, Xingyan Wang, Angeles Fernandez-Gonzalez, S. Alex Mitsialis, Stella Kourembanas, Petr Baranov, Ye Sun

{"title":"Photoreceptors inhibit pathological retinal angiogenesis through transcriptional regulation of Adam17 via c-Fos","authors":"Xudong Wang, Tianxi Wang, Satoshi Kaneko, Emil Kriukov, Enton Lam, Manon Szczepan, Jasmine Chen, Austin Gregg, Xingyan Wang, Angeles Fernandez-Gonzalez, S. Alex Mitsialis, Stella Kourembanas, Petr Baranov, Ye Sun","doi":"10.1007/s10456-024-09912-0","DOIUrl":"10.1007/s10456-024-09912-0","url":null,"abstract":"<div><p>Pathological retinal angiogenesis profoundly impacts visual function in vascular eye diseases, such as retinopathy of prematurity (ROP) in preterm infants and age-related macular degeneration in the elderly. While the involvement of photoreceptors in these diseases is recognized, the underlying mechanisms remain unclear. This study delved into the pivotal role of photoreceptors in regulating abnormal retinal blood vessel growth using an oxygen-induced retinopathy (OIR) mouse model through the c-Fos/A disintegrin and metalloprotease 17 (Adam17) axis. Our findings revealed a significant induction of c-Fos expression in rod photoreceptors, and c-Fos depletion in these cells inhibited pathological neovascularization and reduced blood vessel leakage in the OIR mouse model. Mechanistically, c-Fos directly regulated the transcription of <i>Adam17</i> a shedding protease responsible for the production of bioactive molecules involved in inflammation, angiogenesis, and cell adhesion and migration. Furthermore, we demonstrated the therapeutic potential by using an adeno-associated virus carrying a rod photoreceptor-specific short hairpin RNA against <i>c-fos</i> which effectively mitigated abnormal retinal blood vessel overgrowth, restored retinal thickness, and improved electroretinographic (ERG) responses. In conclusion, this study highlights the significance of photoreceptor c-Fos in ROP pathology, offering a novel perspective for the treatment of this disease.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 3","pages":"379 - 395"},"PeriodicalIF":9.2,"publicationDate":"2024-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140130559","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

Group XIV C-type lectins: emerging targets in tumor angiogenesis 第 XIV 组 C 型凝集素：肿瘤血管生成的新靶点。

IF 9.2 1区医学

Angiogenesis Pub Date : 2024-03-12 DOI: 10.1007/s10456-024-09907-x

Elliott J. Yee, Isaac Vigil, Yi Sun, Robert J. Torphy, Richard D. Schulick, Yuwen Zhu

{"title":"Group XIV C-type lectins: emerging targets in tumor angiogenesis","authors":"Elliott J. Yee, Isaac Vigil, Yi Sun, Robert J. Torphy, Richard D. Schulick, Yuwen Zhu","doi":"10.1007/s10456-024-09907-x","DOIUrl":"10.1007/s10456-024-09907-x","url":null,"abstract":"<div><p>C-type lectins, distinguished by a C-type lectin binding domain (CTLD), are an evolutionarily conserved superfamily of glycoproteins that are implicated in a broad range of physiologic processes. The group XIV subfamily of CTLDs are comprised of CD93, CD248/endosialin, CLEC14a, and thrombomodulin/CD141, and have important roles in creating and maintaining blood vessels, organizing extracellular matrix, and balancing pro- and anti-coagulative processes. As such, dysregulation in the expression and downstream signaling pathways of these proteins often lead to clinically relevant pathology. Recently, group XIV CTLDs have been shown to play significant roles in cancer progression, namely tumor angiogenesis and metastatic dissemination. Interest in therapeutically targeting tumor vasculature is increasing and the search for novel angiogenic targets is ongoing. Group XIV CTLDs have emerged as key moderators of tumor angiogenesis and metastasis, thus offering substantial therapeutic promise for the clinic. Herein, we review our current knowledge of group XIV CTLDs, discuss each’s role in malignancy and associated potential therapeutic avenues, briefly discuss group XIV CTLDs in the context of two other relevant lectin families, and offer future direction in further elucidating mechanisms by which these proteins function and facilitate tumor growth.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"27 2","pages":"173 - 192"},"PeriodicalIF":9.2,"publicationDate":"2024-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11021320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140100898","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