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Open AccessJournal ArticleDOI

The biology of vascular endothelial growth factor

Napoleone Ferrara, +1 more
- 01 Feb 1997 - 
- Vol. 18, Iss: 1, pp 4-25
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TLDR
The establishment of a vascular supply is required for organ development and differentiation as well as for tissue repair and reproductive functions in the adult.
Abstract
The establishment of a vascular supply is required for organ development and differentiation as well as for tissue repair and reproductive functions in the adult1 Neovascularization (angiogenesis) is also implicated in the pathogenesis of a number of disorders These include: proliferative retinopathies, age-related macular degeneration, tumors, rheumatoid arthritis, and psoriasis1,2 A strong correlation has been noted between density of microvessels in primary breast cancers and their nodal metastases and patient survival3 Similarly, a correlation has been reported between vascularity and invasive behavior in several other tumors4–6

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Citations
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Journal ArticleDOI

The biology of VEGF and its receptors.

TL;DR: Vascular endothelial growth factor (VEGF) is a key regulator of physiological angiogenesis during embryogenesis, skeletal growth and reproductive functions and is implicated in pathologicalAngiogenesis associated with tumors, intraocular neovascular disorders and other conditions.
Journal ArticleDOI

Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia

TL;DR: It is confirmed that placental soluble fms-like tyrosine kinase 1 (sFlt1), an antagonist of VEGF and placental growth factor (PlGF), is upregulated in preeclampsia, leading to increased systemic levels of sFlt 1 that fall after delivery, and observations suggest that excess circulating sFelt1 contributes to the pathogenesis of preeClampsia.
Journal ArticleDOI

Vascular endothelial growth factor: basic science and clinical progress.

TL;DR: Vascular endothelial growth factor (VEGF) is an endothelial cell-specific mitogen in vitro and an angiogenic inducer in a variety of in vivo models and is implicated in intraocular neovascularization associated with diabetic retinopathy and age-related macular degeneration.
Journal ArticleDOI

Role of the Vascular Endothelial Growth Factor Pathway in Tumor Growth and Angiogenesis

TL;DR: Recently, an anti-VEGF antibody (bevacizumab), when used in combination with chemotherapy, was shown to significantly improve survival and response rates in patients with metastatic colorectal cancer and thus, validate VEGF pathway inhibitors as an important new treatment modality in cancer therapy.
References
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Journal ArticleDOI

Interleukin 6 Induces the Expression of Vascular Endothelial Growth Factor

TL;DR: It is demonstrated using Northern analysis that treatment of various cell lines with IL-6 for 6-48 h results in a significant induction of VEGF mRNA, and it is shown that the 5′-UTR is important for the expression of V EGF.
Journal ArticleDOI

Vascular endothelial growth factor/vascular permeability factor expression in a mouse model of retinal neovascularization

TL;DR: Data suggest that VEGF/VPF expression in the retina plays a central role in the development of retinal ischemia-induced ocular neovascularization.
Journal ArticleDOI

Increased microvascular permeability and endothelial fenestration induced by vascular endothelial growth factor

TL;DR: The VEGF effect on permeability is unlike that of any other mediator described to date since both muscular venules and capillaries are affected.
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Hypoxia Regulates Vascular Endothelial Growth Factor Gene Expression in Endothelial Cells Identification of a 5′ Enhancer

TL;DR: Using a DNA fragment containing human VEGF promoter sequence, a 28-bp element is identified that is necessary and sufficient to upregulate transcription in response to hypoxia and may be the binding site for certain constitutive binding proteins.
Journal ArticleDOI

Development of retinal vasculature is mediated by hypoxia-induced vascular endothelial growth factor (VEGF) expression by neuroglia

TL;DR: It is proposed that hypoxia caused by the onset of neuronal activity is detected by strategically located populations of neuroglia, first astrocytes, then Muller cells, and in response they secrete VEGF, inducing formation of the superficial and deep layers of retinal vessels, respectively.
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