Angiogenesis最新文献

{"title":"Characterizing pancreatic cancer-associated fibroblast heterogeneity in vascular microphysiological systems","authors":"Charles W. Blackledge,&nbsp;Sarah Gullion,&nbsp;Ian McCabe,&nbsp;Ngan N. K. Van,&nbsp;Arthi Hariharan,&nbsp;Changfei Luan,&nbsp;Xianlu Laura Peng,&nbsp;William J. Polacheck,&nbsp;Jen Jen Yeh,&nbsp;Sarah E. Shelton","doi":"10.1007/s10456-026-10061-9","DOIUrl":"10.1007/s10456-026-10061-9","url":null,"abstract":"<div><p>Pancreatic Ductal Adenocarcinoma (PDAC), one of the deadliest cancer types, is dominated by a tumor microenvironment (TME) that is desmoplastic, immunosuppressive, and generally unresponsive to conventional cancer treatments. Cancer-Associated Fibroblasts (CAFs) are thought to drive many of the features of PDAC that contribute to treatment resistance, yet CAFs exhibit wide phenotypic heterogeneity with unclear biological and clinical implications. Recent work has identified CAF subtypes – tumor-restraining CAFs (RestCAFs) or tumor-promoting CAFs (ProCAFs) – that correlate with overall survival. Therefore, this study aims to identify CAF subtype-dependent functional effects in the TME using 3D microphysiological systems, focusing primarily on their interactions with vasculature. Microfluidic devices including a RestCAF line demonstrated increased levels of vasculogenesis and extracellular matrix remodeling, while devices containing a ProCAF line exhibited increased angiogenic sprouting and differential immune cell recruitment, such as monocyte migration into the TME. This work provides novel insights into the heterogeneous functions of CAFs in the TME and lays important groundwork for the development of CAF-targeted therapies in PDAC.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 3","pages":""},"PeriodicalIF":9.2,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-026-10061-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148209820","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":"An Rnf213-deficient hypoperfusion model reveals Moyamoya-relevant neurovascular remodeling","authors":"Yuanyuan Dai,&nbsp;Xiaoxin Wu,&nbsp;Shuai Li,&nbsp;Xingyang Niu,&nbsp;Jiaoxing Li,&nbsp;Jianhao Lin,&nbsp;Wenli Sheng","doi":"10.1007/s10456-026-10058-4","DOIUrl":"10.1007/s10456-026-10058-4","url":null,"abstract":"<div><p>Moyamoya disease (MMD) is a chronic cerebrovascular disorder characterized by progressive stenosis of the terminal portions of the bilateral internal carotid arteries and their major branches, accompanied by the development of an abnormal vascular network at the base of the brain. Although <i>RNF213</i> is the major susceptibility gene, its relatively low penetrance in MMD suggests that genetic predisposition requires synergistic interaction with environmental stressors to induce the characteristic pathological vascular remodeling. Studies have demonstrated that patients with MMD exhibit mild stenosis of the common carotid artery (CCA) diameter. Furthermore, a reduction in CCA diameter is associated with an increase in cerebral blood volume and a prolongation of mean transit time. Based on this novel clinical finding, we established a mouse model combining <i>Rnf213</i> knockout with bilateral common carotid artery stenosis. These mice exhibited hypoperfusion-induced neurovascular remodeling with moyamoya-relevant features, including cerebral hemorrhage, infarction, and extensive proliferation of fragile microvessels. Mechanistically, <i>RNF213</i> knockdown sensitizes cerebral vessels to hypoperfusion stress and promotes the proliferation and migration of brain microvascular endothelial cells in the absence of shear stress. In conclusion, these results link <i>Rnf213</i> deficiency with mild CCA stenosis under hypoperfusion stress, providing additional insights into the complex systemic manifestations of MMD pathogenesis.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 3","pages":""},"PeriodicalIF":9.2,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148209845","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":"Prevascularized grafts with spatially organized MSC spheroids to accelerate therapeutic angiogenesis in ischemic disease","authors":"Jeonghyun Son,&nbsp;Aruzhan Naren,&nbsp;Hanan Jamal Mohamed,&nbsp;Minjun Ahn,&nbsp;Won Ha,&nbsp;Min Kyeong Kim,&nbsp;Seunggyu Jeon,&nbsp;Byoung Soo Kim,&nbsp;Yoon-Kyoung Cho,&nbsp;Shoji Takeuchi,&nbsp;Hyun-Wook Kang","doi":"10.1007/s10456-026-10059-3","DOIUrl":"10.1007/s10456-026-10059-3","url":null,"abstract":"<div><h3>Objective</h3><p>Ischemic diseases, characterized by impaired blood flow and progressive tissue necrosis, remain a major challenge in regenerative medicine. Surgical revascularization remains the gold standard for restoring blood flow in major vessels, but still shows limited effects on microvascular regeneration. To address this unmet need, various strategies in therapeutic angiogenesis have been explored to induce microvascular formation, including delivery of bioactive molecules, stem cells, or pre-vascularized grafts. However, injection-based approaches often suffer from off-target effects, and conventional implantable grafts lack sufficient angiogenic secretory activity. To address these limitations, we aimed to develop a dual-function prevascularized graft that accelerates neovascularization and promotes vascular integration to restore tissue perfusion in ischemic conditions.</p><h3>Methods and results</h3><p>The graft was engineered by combining a microvascular pattern (µVP) with spatially organized mesenchymal stem cell (MSC) spheroids, fabricated via high-precision coprinting of endothelial cells and MSCs. Optimization of spheroid density and spatial arrangement enhanced VEGF secretion and increased host capillary infiltration nearly two-fold. In a murine critical limb ischemia model, implantation of these engineered grafts achieved a 60% limb salvage rate and reduced limb loss by ~ 15%, representing a 4.5-fold improvement over conventional grafts. Histological and morphometric analyses confirmed reduced muscle degeneration, enhanced neovascularization, and seamless anastomosis between engineered and host vessels.</p><h3>Conclusions</h3><p>These findings demonstrate a dual-functional graft that couples paracrine stimulation with structural vascular support, providing a promising regenerative strategy to promote therapeutic angiogenesis and ischemia therapy, while indicating its potential for preclinical and future clinical applications in ischemic disease.</p><h3>Graphical abstract</h3><div><figure><div><div><picture><source><img></source></picture><span>The alternative text for this image may have been generated using AI.</span></div><div><p>Schematic illustration of engineered grafts designed to enhance secretion and vascular integration, thereby promoting therapeutic angiogenesis and restoring blood perfusion in hindlimb ischemia</p></div></div></figure></div></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 3","pages":""},"PeriodicalIF":9.2,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-026-10059-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148209832","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":"Soluble CD146 reflects altered endothelial and metabolic homeostasis in peripheral artery disease","authors":"Haizam Oubari,&nbsp;Julien Labreuche,&nbsp;Charlotte Reytier,&nbsp;Françoise Dignat-George,&nbsp;Jean-Paul Duong-Van-Huyen,&nbsp;Joseph Emmerich,&nbsp;Pascale Gaussem,&nbsp;Patrick Bruneval,&nbsp;Marcel Blot-Chabaud,&nbsp;Alexandre G. Lellouch,&nbsp;Nathalie Bardin,&nbsp;David M. Smadja","doi":"10.1007/s10456-026-10064-6","DOIUrl":"10.1007/s10456-026-10064-6","url":null,"abstract":"<div><h3>Background</h3><p>Peripheral Arterial Disease (PAD) is a prevalent but underdiagnosed pathology. Soluble CD146 (sCD146) was described as a marker of endothelial dysfunction and vascular congestion.</p><h3>Objective</h3><p>We hypothesize that sCD146 may represent a novel biomarker of PAD. Our objective was to evaluate the association between plasma sCD146 levels and the occurrence and severity of PAD.</p><h3>Methods</h3><p>In this case–control study, 184 Caucasian men with symptomatic PAD were compared to 163 age-matched healthy control patients. PAD diagnosis was confirmed using ankle-brachial index (ABI) and imaging. Plasma sCD146 was quantified using ELISA. Associations with clinical and biochemical parameters were analyzed through multivariable logistic regression models.</p><h3>Results</h3><p>sCD146 level was significantly reduced in PAD patients (mean [95% CI]: 288 ng/mL [269–306]) versus control patients (480 ng/mL [460–500], <i>p</i> &lt; 0.0001). A 10 ng/mL decrease in sCD146 was associated with an age-adjusted odds ratio (OR) of 1.17 (95% CI 1.13–1.22) for PAD, increasing to OR 1.25 (95% CI 1.14–1.36, <i>p</i> &lt; 0.0001) after adjustment for risk factors. sCD146 was not associated with PAD severity (by Fontaine stage). Notably, the association between sCD146 and HDL-C was positively correlated in controls (β = 0.220, <i>p</i> = 0.005), but negatively correlated in PAD patients (β = − 0.156, <i>p</i> = 0.041), with significant interaction (<i>p</i> = 0.002). Age-adjusted OR for PAD was highest in individuals with high HDL-C tertiles (OR = 1.41, 95% CI 1.22–1.63).</p><h3>Conclusion</h3><p>A lower sCD146 concentration is independently associated with PAD. Additionally, an inverse relationship was observed between HDL-C and these patients. These findings suggest that sCD146 may reflect impaired endothelial homeostasis and metabolic dysregulation in PAD, indicating that it could serve as a diagnostic biomarker for the pathology.</p><p><i>Clinical trials registration</i>: NCT00377897.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 3","pages":""},"PeriodicalIF":9.2,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-026-10064-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148209787","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":"Congenital portosystemic shunt with extensive collateralization in an adult with recurrent episodes of hyperammonemic encephalopathy","authors":"David Melville,&nbsp;Mayowa A. Osundiji","doi":"10.1007/s10456-026-10055-7","DOIUrl":"10.1007/s10456-026-10055-7","url":null,"abstract":"","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 3","pages":""},"PeriodicalIF":9.2,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148209843","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":"Transcriptomic characters of cochlear vascular cells with pericyte-driven angiogenetic activity","authors":"Pingting Wang,&nbsp;Yunpei Zhang,&nbsp;Zhiqiang Hou,&nbsp;Jinhui Zhang,&nbsp;Kushal Sharma,&nbsp;Xiaorui Shi","doi":"10.1007/s10456-026-10060-w","DOIUrl":"10.1007/s10456-026-10060-w","url":null,"abstract":"<div><p>The normal structure and function of inner-ear blood vessels, including the microvascular network of the stria vascularis (SV) within the blood-labyrinth barrier (BLB), are essential for auditory function. Despite this, the genetic and molecular characteristics of cochlear vasculature are largely unexplored. In this study, we used single-cell RNA sequencing to profile endothelial cells (ECs) and pericytes (PCs) from the adult mouse cochlea. We found a distinct genetic profile and a higher angiogenic potential than observed in the blood-brain barrier (BBB). Two subclasses of PCs were identified. Type 1 PCs, with high levels of α-smooth muscle actin (<i>Acta2</i>) and <i>Tagln</i>, are located on pre-/post-capillary zones. Type 2 PCs, characterized by low <i>Tagln</i> and high <i>Kcnj8</i>/<i>Abcc9</i> levels, are found specifically in capillary regions. In an ex vivo explant model, both subclasses showed tip-like behavior during sprouting. Ligand-receptor analysis indicated active EC-PC communication. This communication is mediated by adhesive signals, gap junctions, and vesicle trafficking. Using dual fluorescent reporter mouse models, we showed for the first time that PCs can exhibit tip-associated phenotypic plasticity with detectable NG2/PECAM-1 overlap at the sprout front. This <i>tip-associated state</i> may occur from existing cells or progenitors within the vascular niche. Our findings define the molecular signature of cochlear vessels and identify PCs as targets to promote vascular regeneration. This could have implications for hearing restoration when cochlear blood flow is compromised.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 3","pages":""},"PeriodicalIF":9.2,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-026-10060-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148154974","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":"HDAC inhibition reprograms stem cell fate to suppress infantile hemangioma vasculogenesis","authors":"Qiming Chen,&nbsp;Hao Rong,&nbsp;Chao Liu,&nbsp;Jiang Li,&nbsp;Jiawei Zheng,&nbsp;Qian Bian","doi":"10.1007/s10456-026-10057-5","DOIUrl":"10.1007/s10456-026-10057-5","url":null,"abstract":"<div><p>Infantile hemangioma (IH), the most common vascular tumor of infancy, relies on hemangioma stem cells (HemSCs) to drive pathological vasculogenesis during the proliferating phase. While beta-blockers are currently first-line treatment for IH, resistance and rebound growth necessitates novel strategies. Here, we identify histone deacetylase inhibitors (HDACi) as a potential epigenetic drug for IH. The pan-HDAC inhibitor SAHA significantly suppresses in vivo vasculogenesis in a murine IH model. Mechanistically, SAHA selectively blocks the differentiation of HemSCs into pericytes by destabilizing NOTCH3 protein through acetylation-primed ubiquitination and proteasomal degradation, thus disrupting perivascular support which is indispensable for IH vasculogenesis. Furthermore, the blockade of pericyte differentiation by SAHA synergizes with propranolol, which inhibits endothelial differentiation of HemSCs, in a complementary manner. Additionally, SAHA promotes adipogenic differentiation of HemSCs and accelerates IH involution. Collectively, our work highlights the clinical significance of cell fate determination during IH progression, and establishes HDAC inhibition as a novel therapeutic option for IH through targeting pericyte differentiation of HemSCs, which provides a promising enhancement to current treatment strategies of refractory IH.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 3","pages":""},"PeriodicalIF":9.2,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148155044","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":"Endothelialization of bioprosthetic valves: unanswered questions and a roadmap for translational research","authors":"Bo jiang,&nbsp;Hongjun Liu","doi":"10.1007/s10456-026-10056-6","DOIUrl":"10.1007/s10456-026-10056-6","url":null,"abstract":"","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 3","pages":""},"PeriodicalIF":9.2,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-026-10056-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148155060","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":"Portal vein embolization versus radiation lobectomy as pre-treatment for major liver resection for colorectal liver metastases: functional assessment of the future liver remnant","authors":"Khalil Ramdhani,&nbsp;Rosalie C. M. van Rees,&nbsp;Daan Andel,&nbsp;Jeanine M. L. Roodhart,&nbsp;Arthur J. A. T. Braat,&nbsp;Rutger C. G. Bruijnen,&nbsp;Inne H. M. Borel Rinkes,&nbsp;Onno Kranenburg,&nbsp;Marnix G. E. H. Lam,&nbsp;Maarten L. J. Smits,&nbsp;Jeroen Hagendoorn","doi":"10.1007/s10456-026-10049-5","DOIUrl":"10.1007/s10456-026-10049-5","url":null,"abstract":"<div><h3>Introduction</h3><p>Insufficiency of the future liver remnant (FLR) precludes surgery for liver tumors as it is associated with post-hepatectomy liver failure (PHLF). A common strategy to induce pre-operative FLR hypertrophy is portal vein embolization of the tumor bearing liver lobe. More recently, transarterial radio-embolization (radiation lobectomy, RL) has been employed. Direct functional assessment using 99mTc-mebrofenin-hepatobiliary-scintigraphy (HBS) predicts FLR sufficiency more accurately than conventional volume assessment. However, studies describing dynamic functional assessment of the FLR after RL as induction for surgery are currently lacking. This study aims to compare FLR functional changes after PVE and RL.</p><h3>Methods</h3><p>This non-interventional retrospective single-center cohort study was performed between 2016 and 2024. Patients with colorectal liver metastases (CRLM) who underwent PVE or RL because of an insufficient FLR (HBS &lt; 2.7%/min/m²) were included. Induction of sufficient FLR function was the primary outcome.</p><h3>Results</h3><p>Ten PVE- and ten RL-treated patients were included. The median duration to achieve sufficient FLR function was longer for RL- than PVE-treated patients (75 days (64–85) vs 31 days (28–54.5), <i>p</i> = 0.002). RL showed a non-significant higher median functional increase (58.6% vs 51.1%, <i>p</i> = 0.940) and a significantly higher voluminal increase (65.7% vs 36.8%, <i>p</i> = 0.049) compared to PVE. PHLF and resection margins were comparable among groups. There was no 90 day mortality.</p><h3>Conclusion</h3><p>RL represents a feasible alternative to PVE with comparable functional outcomes, particularly in patients with lower baseline FLR function or need for simultaneous tumor control. This warrants prospective studies with optimized RL protocols to better define the functional outcomes and clinical applications of RL versus PVE.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 3","pages":""},"PeriodicalIF":9.2,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13190528/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147980195","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":"An epigenetic switch in vascular phenotype augments anti-tumor immunity","authors":"Dae Joong Kim,&nbsp;Mitchell McGinty,&nbsp;Swetha Anandh,&nbsp;Caroline Riedstra,&nbsp;Yuvraj Sethi,&nbsp;Melanie R. Rutkowski,&nbsp;Andrew C. Dudley","doi":"10.1007/s10456-026-10042-y","DOIUrl":"10.1007/s10456-026-10042-y","url":null,"abstract":"<div><p>The abnormal tumor vasculature can present a barrier to the infiltration of anti-tumor immune cells, which impairs immune surveillance and response to immunotherapy. Here, we show that genetically deleting the epigenetic factor DNA methyltransferase 1 (<i>Dnmt1</i>) in endothelial cells (ECs) reduces angiogenesis while imparting profound changes to the tumor immune microenvironment (TIME), including increased proportions of CD4⁺ memory T cells and NK cells. Depleting CD4⁺ T cells, or blocking lymphocyte egress from the lymph nodes, rescues tumor growth in mice with conditional deletion of <i>Dnmt1</i> in ECs (<i>Dnmt1</i>^iECKO) and dramatically shortens overall survival, whereas NK cells are dispensable. Tumors implanted in <i>Dnmt1</i>^iECKO mice show reduced vascular branching, elevated expression of VCAM1, increased vessel-associated T cells, and a shift in vascular specification, including increased proportions of immune-permissive post-capillary venules (PCVs) and interferon-stimulated ECs (IFN-ECs). Deleting <i>Dnmt1</i> in EC cultures strikingly potentiates responses to combinations of IFNγ and TNFα and, notably, up-regulates important T-cell co-stimulatory molecules for memory CD4⁺ T cells, including <i>Icosl</i>, <i>Cd40</i>, and <i>Tnfsf4</i>. Finally, immune checkpoint blockade (ICB) administered to <i>Dnmt1</i>^iECKO mice with experimental melanoma lung metastasis reduces tumor burden, with some mice showing tumor eradication. Our findings identify endothelial <i>Dnmt1</i> as a key regulator of vascular-mediated anti-tumor immunity, providing a rationale for integrating epigenetic modulation of the vasculature with cancer immunotherapy regimens.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 3","pages":""},"PeriodicalIF":9.2,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13186828/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147969911","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}