Angiogenesis最新文献

{"title":"YTHDF3 promotes angiogenesis in endometriosis by enhancing the translation efficiency of PFKFB3","authors":"Xiaosa Li,&nbsp;Jiale Wang,&nbsp;Liang Yuan,&nbsp;Yuqi Wang,&nbsp;Jinzhi Wei,&nbsp;Ping Li,&nbsp;Runxin Wang,&nbsp;Xingyan Xu,&nbsp;Qiuwen Mai,&nbsp;Junxiu Liu,&nbsp;Huiping Lin,&nbsp;Xiaodong Fu","doi":"10.1007/s10456-026-10095-z","DOIUrl":"10.1007/s10456-026-10095-z","url":null,"abstract":"<div><p>Angiogenesis plays a critical role in the progression of endometriosis, with enhanced glycolysis accelerating pathological angiogenesis. Prior research has identified a central role for N6-methyladenosine (m6A) modification in regulating glycolytic processes. This study investigates the involvement of m6A-mediated mechanisms in the regulation of glycolysis and angiogenesis in endometriosis. Here, we report that PFKFB3 is significantly upregulated in vascular endothelial cells of ectopic endometrial tissues from humans and mice, correlating with elevated expression of YTHDF3. Specific deletion of <i>Ythdf3</i> in endothelial cells reduces PFKFB3 protein levels and suppresses angiogenesis in ectopic endometrial lesions. Mechanistically, PFKFB3 mRNA displays increased m6A modifications in endometrial microvascular endothelial cells (EMECs). METTL3 enhances m6A modification of PFKFB3 mRNA, which is recognized by YTHDF3, promoting PFKFB3 translation and glycolytic activity, thus facilitating tube formation, migration, and proliferation of ovarian microvascular endothelial cells (OMECs). Moreover, estrogen upregulates both METTL3 and PFKFB3 via the estrogen receptor ERα. Collectively, these findings establish the YTHDF3-m6A-PFKFB3 pathway as a critical driver of angiogenesis in endometriosis, suggesting that targeting this pathway represents a promising therapeutic strategy.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 4","pages":""},"PeriodicalIF":11.2,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149029621","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":"Endothelial Epac1 facilitates YAP/TAZ controlled melanoma growth and angiogenesis","authors":"Yohanes Cakrapradipta Wibowo,&nbsp;Nan Ma,&nbsp;Yonggang Ren,&nbsp;Julio Cordero,&nbsp;Johannes Gahn,&nbsp;Zihao Chen,&nbsp;Magdalena Levay,&nbsp;Roxana Ola,&nbsp;Yuxi Feng,&nbsp;Gergana Dobreva,&nbsp;Harald Langer,&nbsp;Thomas Wieland,&nbsp;Christiane Vettel,&nbsp;Sepp Jansen","doi":"10.1007/s10456-026-10080-6","DOIUrl":"10.1007/s10456-026-10080-6","url":null,"abstract":"<div><p>The RapGEF Epac1 has emerged as an important modulator of pro-angiogenic signalling pathways, including VEGF/VEGFR2. However, its specific role in tumor angiogenesis has remained unexplored. Here, we identify endothelial Epac1 as a critical driver of melanoma angiogenesis. Analysis of patient-derived melanomas revealed that Epac1 is markedly upregulated in tumor endothelial cells. Using both global and endothelial-specific <i>Epac1</i> knockout mouse models, we demonstrate that <i>Epac1</i> deletion reduced melanoma growth and vascularization following subcutaneous melanoma cell inoculation. Transcriptome profiling of tumor-associated endothelial cells from <i>Epac1</i>-deficient mice showed broad downregulation of pro-angiogenic and YAP/TAZ target genes. This was corroborated in vitro using an <i>Epac1</i> knockout endothelial cell line, where VEGFR2 expression, YAP/TAZ nuclear translocation, and YAP/TAZ target gene transcription were all suppressed. Consistently, <i>Epac1</i> deletion impaired VE-cadherin/VEGFR2 interaction, VEGF-dependent nuclear YAP/TAZ and transcriptional activity, and abolished endothelial cell alignment in response to shear stress. Collectively, our results reveal Epac1 as a central modulator of VEGFR2 and YAP/TAZ signalling, integrating angiogenic and mechanosensory cues during melanoma vascularization.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 4","pages":""},"PeriodicalIF":11.2,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-026-10080-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149029587","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":"Angiogenesis-promoting properties of phosphorylcholine mimetic nanoparticles","authors":"Mona Moradi,&nbsp;Bijay K. Poudel,&nbsp;Erika Hooker,&nbsp;Mozhgan Aghajanzadeh-Kiyaseh,&nbsp;Diana Rusu,&nbsp;May Griffith,&nbsp;Bruno Larrivée","doi":"10.1007/s10456-026-10094-0","DOIUrl":"10.1007/s10456-026-10094-0","url":null,"abstract":"<div><p>Therapeutic angiogenesis aims to re-establish the blood supply to ischemic tissues. We developed a novel strategy in which nanoparticles (NPs) made from polymers of an artificial methacrylated phosphorylcholine (polyMPC) were used directly to stimulate angiogenesis. PolyMPC NPs under 150 nm were internalized by cultured human umbilical vein endothelial cells (HUVECs) in vitro, stimulating their proliferation and angiogenic responses. In vivo, the subcutaneous implantation of polyMPC NPs delivered within Matrigel plugs in mice produced a significant pro-angiogenic response. PolyMPC NPs were also shown to induce expansion of human cord blood and bone marrow endothelial progenitor cells. Mechanistically, internalization of polyMPC NPs by HUVECs induced the recruitment of protein kinase C (PKC) to the plasma membrane leading to its activation. RNA sequencing revealed that polyMPC NPs upregulated pro-angiogenic growth factors in HUVECs, including VEGF and FGF2. Delivered polyMPC NPs could be retained in tissues for extended periods, stimulating endogenous production of pro-angiogenic growth factors for therapeutic effects. Overall, we demonstrated that angiogenesis therapy based on polyMPC NPs could be a novel alternative, cost-effective method to treat ischemic vascular pathologies.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 4","pages":""},"PeriodicalIF":11.2,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149029560","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: MCC links Wnt/PCP signaling to endothelial polarity and vascular remodeling","authors":"Valentin Delobel,&nbsp;Béatrice Jaspard,&nbsp;Malvina Salami,&nbsp;Marion Camoin,&nbsp;Claire Peghaire,&nbsp;Juliette Vaurs,&nbsp;Romain Boulestreau,&nbsp;Maija Kohonen-Corish,&nbsp;Alexandre Dubrac,&nbsp;Thierry Couffinhal,&nbsp;Cécile Duplàa","doi":"10.1007/s10456-026-10086-0","DOIUrl":"10.1007/s10456-026-10086-0","url":null,"abstract":"","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 4","pages":""},"PeriodicalIF":11.2,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149007816","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":"Regulation of PDGF-BB signaling in placental pericytes by soluble PDGFRβ isoforms: implications for fetoplacental vascular development","authors":"Audra R. Barnes-Lanier,&nbsp;Emily C. Duggan,&nbsp;Reese A. Dunkenberger,&nbsp;Chloe V. Lessard,&nbsp;Christopher C. Cosma,&nbsp;Chase R. Steele,&nbsp;Sarah V. Taylor,&nbsp;Jordan A. Darden,&nbsp;Megan D. Whitham,&nbsp;Allison R. Durica,&nbsp;John C. Chappell","doi":"10.1007/s10456-026-10091-3","DOIUrl":"10.1007/s10456-026-10091-3","url":null,"abstract":"<div><p>Vascular remodeling within the developing fetus and placenta is essential for supporting the growth and function of emerging tissues and organs. Pericytes (PCs) play a central role in stabilizing and maturing microvascular networks by extending along endothelial cells (ECs) and reinforcing vessel integrity. In the placenta, as in other organs, PC–EC communication is mediated in part by platelet-derived growth factor-BB (PDGF‑BB) signaling, which governs PC differentiation, proliferation, migration, and survival, ultimately enabling their recruitment and retention along capillaries. In this study, we identified progressive PC investment along feto‑placental capillaries in both murine and human tissues across gestation, supported by morphological and molecular evidence. Placental PCs displayed phenotypic heterogeneity comparable to that observed in the brain and heart, suggesting conserved diversity across organ systems. In addition to characterizing PC dynamics, we examined the expression of recently identified soluble PDGF Receptor-β (sPDGFRβ) isoforms. These variants were detected at the protein and transcript levels in mouse and human placentas, as well as in a murine trophoblast‑embryonic stem cell (TESC) differentiation model that recapitulates aspects of early placental vascular development. Within this model, sPDGFRβ expression was independent of ADAM10 activity and exogenous growth factors during early vessel formation but was markedly upregulated during hypoxia. To assess how elevated sPDGFRβ might influence PDGF‑BB signaling, we exposed TESC‑derived vascular networks to excess PDGF‑BB with or without a sPDGFRβ mimetic. PDGF‑BB alone reduced full‑length PDGFRβ levels while increasing receptor phosphorylation, consistent with known ligand‑induced regulatory mechanisms. Inclusion of the sPDGFRβ mimetic shifted these responses toward baseline, suggesting a potential modulatory or feedback role for soluble receptor variants. Together, these findings demonstrate that PCs are progressively recruited to placental capillaries and exhibit diverse phenotypes during development, and that soluble PDGFRβ isoforms may modulate PDGF‑BB signaling in a manner sensitive to oxygen tension. Understanding these mechanisms provides insight into the regulation of placental vascular maturation and may inform strategies to improve human health by targeting disorders rooted in impaired placental development.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 4","pages":""},"PeriodicalIF":11.2,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541826/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886043","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":"Intimal hyperplasia and adventitial angiogenesis originating from veins are vascular remodelling responses in large vessels after major lower extremity trauma induced ischemia","authors":"Adas Cepas,&nbsp;Paavo Saarela,&nbsp;Tuomas Komulainen,&nbsp;Tero Järvinen,&nbsp;Juha Kiiski,&nbsp;Ilkka Kaartinen","doi":"10.1007/s10456-026-10089-x","DOIUrl":"10.1007/s10456-026-10089-x","url":null,"abstract":"<div><h3>Background</h3><p>Total paucity exists on how large human blood vessels respond to ischemia. We explored the human vascular response to trauma-induced ischemia, with a particular focus on vascular wall remodelling.</p><h3>Methods</h3><p>Arterial and venous wall samples were analysed from 40 patients undergoing soft tissue free flap reconstruction following lower extremity trauma. Patients were stratified into an early reconstruction group (median 6 days post-injury (IQR 4–8); n = 26) after high-energy lower extremity open fracture, and a late reconstruction group (median 54 days post-injury (IQR 31–155); n = 14) operated due to fracture non-union or fracture related infection. Injury-site arterial and venous biopsy samples were collected at the anastomosis site during reconstruction, while control samples were obtained from intact blood vessels at free flap donor sites. Quantitative histological and immunohistochemical analyses were performed using QuPath software.</p><h3>Results</h3><p>The cohort consisted predominantly of working-age males (median age: early group 44 years, late 50 years; <i>p </i>= 0.72). Arterial intimal hyperplasia was significantly greater at injury sites than in the control arteries in both groups. Venous intimal thickening exceeded control levels by more than threefold. Adventitial angiogenesis was primarily observed in veins in the early reconstruction group, and it was more pronounced in both arteries and veins of the late group compared to the early group.</p><h3>Conclusions</h3><p>Our findings demonstrate that major lower extremity trauma and trauma-induced ischemia trigger active remodelling across all layers of the vascular wall. The most prominent structural changes are linked to rapid onset of intimal hyperplasia and adventitial angiogenesis originating from the venous system.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 4","pages":""},"PeriodicalIF":11.2,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541956/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148885987","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":"Ocular gene therapy targeting retinal angiogenesis and vascular leakage: translational and clinical evidence from a systematic review and meta-analysis","authors":"Kai-Yang Chen,&nbsp;Hoi-Chun Chan,&nbsp;Chi-Ming Chan","doi":"10.1007/s10456-026-10050-y","DOIUrl":"10.1007/s10456-026-10050-y","url":null,"abstract":"<div><h3>Introduction</h3><p>Retinal diseases driven by pathological angiogenesis and vascular leakage, including neovascular age-related macular degeneration and diabetic retinopathy, impose substantial visual and treatment burdens because current anti-vascular endothelial growth factor (anti-VEGF) therapy requires repeated intravitreal administration. Ocular gene therapy can provide durable intraocular expression of therapeutic proteins and sustained pathway-level disease control.</p><h3>Methods</h3><p>This systematic review and meta-analysis was prospectively registered in the International Prospective Register of Systematic Reviews (PROSPERO) and conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines. PubMed, Scopus, Web of Science, ScienceDirect, and the Cochrane Library were searched from inception to April 21, 2026. Eligible studies included preclinical, in vitro, and clinical investigations of gene-based interventions targeting retinal angiogenesis, vascular permeability, or related anatomical and treatment-burden outcomes. Random-effects meta-analyses were performed using standardized mean differences (SMDs), mean differences (MDs), and logit event rates.</p><h3>Results</h3><p>Twenty-five studies were included. Preclinical gene therapy significantly reduced pathological neovascularization, with a pooled standardized mean difference (SMD) of −1.16 (95% confidence interval [CI], −1.48 to −0.84; p &lt; 0.001) and negligible heterogeneity (I² = 0%). Vascular leakage was also significantly reduced across preclinical experimental studies, with a pooled mean difference (MD) of 0.215 (95% CI, 0.178–0.251; p &lt; 0.001; I² = 0%) after directional harmonization. In clinical cohorts, ocular gene therapy significantly reduced central subfield thickness (CST) by −55.30 μm (95% CI, −72.58 to −38.03; p &lt; 0.001) and was associated with reduced anti-vascular endothelial growth factor (anti-VEGF) treatment burden, with a pooled logit event rate of 0.62 (95% CI, 0.20–1.04; p = 0.0039), corresponding to a pooled proportion of approximately 65% of participants meeting study-specific criteria for reduced supplemental anti-VEGF use.</p><h3>Conclusion</h3><p>Ocular gene therapy shows strong preclinical anti-angiogenic and anti-permeability effects, with emerging clinical evidence of anatomical improvement and reduced anti-VEGF treatment burden in neovascular retinal disease cohorts. Larger disease-specific randomized trials are required to confirm long-term efficacy, safety, and patient selection.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 4","pages":""},"PeriodicalIF":11.2,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13529909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863179","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":"Evaluating the endothelial glycocalyx from bench to bedside: a translational framework for microvascular assessment","authors":"Hiroyuki Tomita,&nbsp;Akio Suzuki,&nbsp;Hideshi Okada","doi":"10.1007/s10456-026-10084-2","DOIUrl":"10.1007/s10456-026-10084-2","url":null,"abstract":"<div><p>The endothelial glycocalyx (eGCX) plays a crucial role in mechanotransduction, maintaining vascular barrier integrity, and facilitating leukocyte–endothelial crosstalk. However, accurately quantifying it is challenging due to fragmented methodologies. As the eGCX is a highly hydrated, labile layer that readily collapses upon chemical fixation and dehydration, reported thickness values span orders of magnitude depending on the specific measurement principle employed. Consequently, relying on single-metric claims risks both false-positive and false-negative conclusions. Compounding this challenge, eGCX composition, morphology, and injury responses vary significantly across organs and vascular beds. This spatial heterogeneity is a factor that standard static in vitro cultures fundamentally fail to recapitulate. To overcome these limitations, we present a cross-platform evaluation framework organized around three orthogonal axes: structure (coverage, penetrability, and component localization), function (permeability and perfusion), and turnover (shedding versus synthesis). We delineate how each readout corresponds to a distinct physical sub-compartment, critically appraising methods that include confocal lectin staining, rapid-freeze electron microscopy (EM), atomic force microscopy (AFM), transendothelial resistance, intravital exclusion-zone imaging, perfused boundary region analysis, and circulating shedding biomarkers. For each platform, including in vitro, in vivo, and clinical settings, we propose minimal yet robust endpoint packages that integrate assay intent, organ context, and hemodynamic covariates. This approach shifts the field toward convergent, translatable inference for eGCX-targeted therapeutics. Beyond cataloguing techniques, the central contribution of this framework is the explicit mapping of each commonly used readout to the specific physical sub-compartment it interrogates, coupled with organ- and vascular-compartment-aware prioritization, so that convergent agreement among orthogonal structural, functional, and turnover measurements—rather than any single value—becomes the basis for falsifiable, translatable inference.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 4","pages":""},"PeriodicalIF":11.2,"publicationDate":"2026-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13499780/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148787285","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":"CXCL12/CXCR4 signaling governs ischemic neurovascular pathophysiology and repair: a multidimensional contextual analysis","authors":"Shahram Eisa-Beygi,&nbsp;Hao Wu,&nbsp;Kui Cui,&nbsp;Kulandaisamy Arulsamy,&nbsp;Bo Zhu,&nbsp;Beibei Wang,&nbsp;Bandana Singh,&nbsp;Krishan Gupta,&nbsp;Jianing Gao,&nbsp;Scott Wong,&nbsp;Joyce Bischoff,&nbsp;Hanqiang Deng,&nbsp;Hong Chen","doi":"10.1007/s10456-026-10074-4","DOIUrl":"10.1007/s10456-026-10074-4","url":null,"abstract":"<div><p>Ischemic stroke is a global health crisis necessitating targeted therapeutic strategies. Central to post-stroke pathology and repair is the CXCL12 signaling axis. In this review, we discuss the context-dependent roles of CXCL12 and its canonical receptor, CXCR4, within the post-ischemic microenvironment. The CXCL12/CXCR4 axis exhibits a temporal duality across the evolution of the neurovascular lesion; however, current evidence necessitates moving beyond a strictly binary framework. While the acute phase involves pathological cascades, such as blood-brain barrier disruption and leukocyte infiltration, the axis is simultaneously essential for recruiting protective innate immune subsets. During subsequent subacute and chronic phases, it governs essential restorative processes, including neurogenesis, angiogenesis, and remyelination. This complex temporal shift is mediated by the interplay between distinct CXCL12 isoforms and the regulatory influence of the atypical receptor ACKR3/CXCR7. Furthermore, these endogenous repair mechanisms exhibit synergies with non-pharmacological interventions, notably environmental enrichment and remote ischemic postconditioning. Our multidimensional model suggests that the functional outcome of CXCL12/CXCR4 signaling is determined by the intersection of timing, cell type, receptor availability, and adaptive responses to physiological stimuli. We synthesize fundamental mechanistic data with translational insights to evaluate the therapeutic potential of this axis and the pharmacological barriers to future regenerative strategies.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 4","pages":""},"PeriodicalIF":11.2,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148783169","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":"Immortalized smooth muscle cells enhance in vitro vasculogenesis","authors":"Mohammad R. Nikmaneshi,&nbsp;Lennard M. Weide,&nbsp;Noel-Adrian Hollosi,&nbsp;Marc A. Höll,&nbsp;Nemo Noeh,&nbsp;Franciele Filardi Cimino Silva,&nbsp;Dan G. Duda,&nbsp;Lance L. Munn","doi":"10.1007/s10456-026-10083-3","DOIUrl":"10.1007/s10456-026-10083-3","url":null,"abstract":"<div><p>De novo vessel formation (vasculogenesis) in vitro is a key step in tissue engineering to preserve tissue viability for long-term assays and testing therapeutic agents. However, in vitro vasculogenesis is often unreliable due to differences in vascular-supporting cells, including endothelial cells and stromal cells such as smooth muscle cells (SMCs) and fibroblasts. Here, we developed a robust co-culture system of HUVECs and SMCs to generate stable vascular networks capable of maintaining tissue viability over extended periods. Given that SMC plasticity is a major limitation in supporting endothelial network formation, we systematically evaluated the effects of passage number, confluency, and freezing on primary SMC function. To overcome this limitation, we generated immortalized supportive SMCs, which preserved their vasculogenic gene program and functional capacity even at high passage. In addition, we identified and validated key genes associated with endothelial support, including CD248, C3, and FBLN1, all essential for vasculogenesis. Immortalized SMCs consistently maintained expression of these genes and supported robust vessel formation under variable culture conditions. Collectively, this study demonstrates that immortalized SMCs provide a stable, reproducible platform for endothelial–SMC co-cultures, enabling long-term vascularized tumor models suitable for functional studies and therapeutic screening.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"29 4","pages":""},"PeriodicalIF":11.2,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-026-10083-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148783168","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}