ANGIOGENESIS血管生成
ANGIOGENESIS(英文缩写 ANGIOGENESIS),ISSN 0969-6970,eISSN 1573-7209,中文译名:血管生成 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 10.658 | Q1 |
| 2022 | 9.800 | Q1 |
| 2023 | 9.200 | Q1 |
| 2024 | 9.200 | Q1 |
| 2025 | 11.200 | Q1 |
ANGIOGENESIS 最新收录文献
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1. {"_":"VEGFb attenuates LPS-induced acute lung injury via antagonizing the VEGFa/VEGFR2 signaling pathway.","sub":["165","165"]}
1. {"_":"VEGFb通过拮抗VEGFa/VEGFR2信号通路减轻LPS诱导的急性肺损伤。","sub":["165","165"]}PMID:日期:2026-10-04Vascular endothelial growth factor (VEGF) plays a central role in the pathogenesis of acute lung injury (ALI) and its severe form, acute respiratory distress syndrome (ARDS), yet targeted therapies for these conditions remain elusive. This study identified the VEGF-A splice variant VEGFb as a crucial endogenous protector against ALI/ARDS. In patients, the circulating ratio of VEGFb to total VEGF-A was significantly reduced and correlated inversely with disease severity. In murine models of LPS-induced ALI, administration of exogenous VEGFb alleviated pulmonary edema, inflammation, and injury, whereas its neutralization exacerbated damage. Mechanistically, VEGFb functioned as a competitive antagonist, selectively inhibiting VEGFa-induced phosphorylation of VEGFR2 at tyrosine 1175. This blockade suppressed the downstream PI3K/AKT/eNOS permeability pathway, reducing SRC-mediated VE-cadherin phosphorylation and thereby enhancing endothelial barrier integrity. Additionally, VEGFb downregulated the chemokine CCL2, limiting monocyte-endothelial adhesion through a distinct anti-inflammatory mechanism. Our findings established VEGFb as a key endogenous stabilizer of the vascular barrier, acting via dual pathways-direct junctional reinforcement and anti-inflammatory activity-and highlighted its potential as both a biomarker and a therapeutic agent for ALI/ARDS. This work revealed the critical balance of VEGF splicing variants in vascular homeostasis and offers a novel strategy for treating vascular barrier dysfunction in critical lung diseases.
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2. Myeloid deficiency of RORα exacerbates lipid dysregulation and laser-induced choroidal neovascularization.
2. 髓系细胞RORα缺失加剧脂质代谢紊乱及激光诱导的脉络膜新生血管形成PMID:日期:2026-09-25Dysregulated lipid and cholesterol metabolism is implicated in the pathogenesis of age-related macular degeneration (AMD), a leading cause of vision loss. Retinoic acid receptor-related orphan receptor alpha (RORα) is a lipid-sensing nuclear receptor genetically associated with neovascular AMD. We investigated the role of RORα in regulating AMD-like pathologies and laser-induced choroidal neovascularization (CNV) through mediating myeloid cell lipid homeostasis and function. Both systemic (Rora) and myeloid-specific (Rora;LysMCre) RORα deficient mice exhibited fundus lesions with aging, and exacerbated CNV with chronic subretinal inflammation, with subretinal accumulation of lipid-laden activated microglia/macrophages, and increased levels of pro-inflammatory cytokines. RORα-deficient macrophages showed enhanced lipid droplet formation and upregulation of peroxisome proliferator-activated receptor gamma (PPARγ), a lipogenic RORα target gene. Pharmacological inhibition of RORα in cultured macrophage recapitulated the effects of RORα deficiency on lipid enrichment and inflammation, whereas PPARγ inhibition in RORα deficient mice partially reversed the effects on laser-induced CNV, lipid accumulation and inflammation. Additionally, migratory chemokine receptors, including CX3CR1 and CD47, were downregulated in RORα-deficient myeloid cells, contributing to impaired elimination of inflammatory cells from the subretinal space. These findings identify RORα as a critical transcriptional regulator that links lipid dysregulation to persistent subretinal inflammation and pathological CNV highly relevant in AMD.
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3. Lysed erythrocyte membranes metabolically prime endothelial cells for angiogenesis.
3. 裂解的红细胞膜通过代谢启动内皮细胞促进血管生成PMID:日期:2026-09-25Endothelial dysfunction is a hallmark of pathological angiogenesis and associated with erythrocyte extravasation and lysis. Whether mediators released from lysed erythrocytes instruct endothelial cells (ECs) for new vessel formation is unknown. Here, we show that the membrane fraction of lysed erythrocytes activates inflammatory endothelial gene transcription and metabolically reprograms ECs to promote angiogenic sprout formation. Alterations in endothelial glucose metabolism occurred downstream of NFκB p65 activation by extracellular ATP via fast-acting endothelial P2X7 receptors and also involved ATP-mediated adenylyl cyclase activation and cyclic AMP generation via P2RY11. Overexpression and acetylation of histone 3 at lysine 27 of NR4A1 was identified as anti-inflammatory control mechanism and angio-metabolic switch activating VEGF, PFKFB3 and other AP-1 dependent gene transcription programs. The angiogenic potential of lysed erythrocyte membranes from patients with peripheral artery disease was impaired and could be restored by inhibiting endothelial phosphodiesterase 4 to prevent endothelial cAMP degradation. Our findings uncover that erythrolysis metabolically primes ECs for angiogenesis and that targeting endothelial cAMP generation may be a promising strategy to restore endothelial angiogenic functions.
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4. YTHDF3 promotes angiogenesis in endometriosis by enhancing the translation efficiency of PFKFB3.
4. YTHDF3通过提高PFKFB3的翻译效率促进子宫内膜异位症中的血管生成PMID:日期:2026-09-23Angiogenesis 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 Ythdf3 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.
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5. Endothelial Epac1 facilitates YAP/TAZ controlled melanoma growth and angiogenesis.
5. 内皮细胞中的Epac1促进YAP/TAZ调控的黑色素瘤生长和血管生成PMID:日期:2026-09-23The 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 Epac1 knockout mouse models, we demonstrate that Epac1 deletion reduced melanoma growth and vascularization following subcutaneous melanoma cell inoculation. Transcriptome profiling of tumor-associated endothelial cells from Epac1-deficient mice showed broad downregulation of pro-angiogenic and YAP/TAZ target genes. This was corroborated in vitro using an Epac1 knockout endothelial cell line, where VEGFR2 expression, YAP/TAZ nuclear translocation, and YAP/TAZ target gene transcription were all suppressed. Consistently, Epac1 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.
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6. Angiogenesis-promoting properties of phosphorylcholine mimetic nanoparticles.
PMID:日期:2026-09-23Therapeutic 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.
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7. Correction: MCC links Wnt/PCP signaling to endothelial polarity and vascular remodeling.
PMID:日期:2026-09-19该文献暂无摘要。
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8. Regulation of PDGF-BB signaling in placental pericytes by soluble PDGFRβ isoforms: implications for fetoplacental vascular development.
8. 可溶性PDGFRβ亚型对胎盘周细胞中PDGF-BB信号通路的调控：对胎儿胎盘血管发育的影响PMID:日期:2026-09-03Vascular 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.
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9. Intimal hyperplasia and adventitial angiogenesis originating from veins are vascular remodelling responses in large vessels after major lower extremity trauma induced ischemia.
PMID:日期:2026-09-03Total 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. 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. The cohort consisted predominantly of working-age males (median age: early group 44 years, late 50 years; p = 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. 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.
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10. Ocular gene therapy targeting retinal angiogenesis and vascular leakage: translational and clinical evidence from a systematic review and meta-analysis.
10. 针对视网膜血管生成和血管渗漏的眼部基因治疗：来自系统综述和荟萃分析的转化和临床证据PMID:日期:2026-08-31Retinal 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. 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. 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 < 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 < 0.001; I = 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 < 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. 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.