Vascular endothelial growth factor
Vascular endothelial growth factor (VEGF) is a family of secreted Signaling proteins that regulate blood-vessel development, angiogenesis, vascular permeability, and endothelial-cell survival.
Vascular endothelial growth factor (VEGF) is a family of secreted Signaling proteins that regulate blood-vessel development, angiogenesis, vascular permeability, and endothelial-cell survival. In humans, the term commonly refers to VEGF-A, the principal product of the VEGFA gene. VEGF-A is induced by tissue hypoxia, in part through hypoxia inducible factor 1 subunit alpha (HIF-1α), and is released by endothelial cells, stromal cells, Macrophages, tumor cells, and other cell types.
VEGF primarily acts through the tyrosine-kinase receptors VEGFR-1 and VEGFR-2 on vascular endothelial cells. Receptor activation stimulates intracellular pathways controlling endothelial-cell proliferation, migration, survival, extracellular-matrix remodeling, and vascular permeability. These processes are essential for wound repair and normal vascular development but can also promote pathological angiogenesis in Cancer, diabetic retinopathy, neovascular Age-related macular degeneration, and other inflammatory or ischemic disorders. VEGF Signaling also interacts with inflammation, reactive oxygen species, cytokines such as interleukin-6 (IL-6), transforming growth factor-β (TGF-β) pathways, and the tumor microenvironment.
VEGF is therefore an important therapeutic target. Anti-VEGF antibodies, receptor-trap proteins, and other VEGF-neutralizing agents inhibit abnormal vessel growth or permeability. In ophthalmology, these agents are administered by intravitreal injection for retinal vascular diseases; in oncology, anti-angiogenic treatment may be used as part of combination Therapy. Excessive suppression of VEGF can, however, affect normal vascular homeostasis and may be associated with treatment-related adverse effects.
- Diffusion histogram analysis predicts progression-free survival in contrast enhancing recurrent IDH mutant gliomas treated with bevacizumab. PMID 42717134
Where the papers sit
13 papers study vascular endothelial growth factor directly. The themes below are drawn from those 13.
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VEGF Angiogenesis Therapies : VEGF modulation spans regenerative delivery of angiogenic factors and anti-VEGF treatment of retinal disease, glioma and macular degeneration. Bevacizumab and aflibercept recur alongside retinal neovascularization, edema and progression-free survival. 7 papers · 53.8%
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Cancer Angiogenesis and Immunity : VEGF targeting is moving toward immune combination strategies such as PD-L1/VEGF bispecific antibodies, while targeted delivery and ligand blockade address tumor growth. Proliferation, migration and cytokine-defined immune state recur as readouts. 4 papers · 30.8%
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Wound Healing and Scar Reduction : Topical and hydrogel approaches are being used to improve vascularization while limiting reactive oxygen species and scar formation. VEGF-associated neovascularization and collagen deposition recur as healing endpoints. 2 papers · 15.4%
Recent Findings on vascular endothelial growth factor
VEGF Angiogenesis Therapies: Bevacizumab treatment in recurrent IDH-mutant glioma showed longer progression-free survival with higher pretreatment ADC-L, but ADC-L did not predict overall survival 42717134Sep. Chronic pseudophakic cystoid macular oedema showed variable treatment timelines, with shorter observed resolution after corticosteroid escalation than anti-VEGF therapy, although non-randomized subgroups limit comparison 42640292Aug. Aflibercept 8 mg produced low newly coded intraocular inflammation risk over one year, but the absence of an active comparator prevents definitive safety conclusions 42576020Aug. Biomaterials increasingly control VEGF activity through sustained neutralizing-antibody delivery, synchronized VEGF and hesperadin release, or phased VEGF, FGF-2, and PDGF presentation, improving pathological retinal angiogenesis suppression, myocardial repair, or in vitro vascular network formation 42555755Aug42492872Jul42447931Jul. In colorectal cancer, MALAT1 overexpression associated with increased VEGF alongside NF-κβ/TGF-β signaling and altered apoptotic proteins, supporting further study of VEGF-linked regulatory networks 42371822Jun.
Cancer Angiogenesis and Immunity: PD-L1/VEGF bispecific blockade and smaller VEGF-binding ligands are advancing targeted approaches to angiogenesis and tumor growth. PLVBP bound PD-L1 and VEGF165 with sub-nanomolar affinities and suppressed VEGF-induced HUVEC proliferation and migration, while the D6 peptide slowed gastric tumor xenograft progression comparably to bevacizumab but required higher, repeated dosing 42269274Jun42545946Aug. Plasma VEGF accompanied cytokine and chemokine patterns associated with head and neck squamous cell carcinoma immunophenotypes, including immune desert, immune excluded, and immune inflamed states 42684559Sep. GLG1-modified nanoparticles delivered VEGF/BMP2 plasmids to bone, enhancing angiogenesis, osteogenic differentiation, trabecular microstructure, and bone strength in ovariectomized rats without systemic toxicity 42508511Jul. These findings favor combination therapy and targeted delivery, while their differing models and endpoints leave clinical effectiveness unresolved.
Wound Healing and Scar Reduction: VEGF-enhanced vascularization combined with control of oxidative stress or collagen deposition improved experimental wound repair and reduced scarring. A RADA16/VEGF/MnO2@GelMA composite hydrogel promoted functional neovascularization while manganese dioxide nanozyme scavenged reactive oxygen species and restrained excessive collagen deposition in full-thickness rat wounds 42673945Aug. Topical Cinnamon zeylanicum accelerated burn healing in rats, increased early serum VEGF levels, and improved re-epithelialization, granulation tissue, collagen fiber synthesis, and cell multiplication 42556083Aug. The direction is toward local formulations that coordinate angiogenesis with redox control and scar inhibition.
Written from 13 PubMed abstracts, each one cited by PMID above. Published: 2026-08-20. Last written: 2026-09-11 by GPT. Drafted by language models from published abstracts; not medical advice.