scholarly journals Inflammatory Choroidal Neovascularisation

2021 ◽  
pp. 1-3
Author(s):  
Priyanka MS ◽  
◽  
Amber Kumar ◽  

Inflammatory choroidal neovascularization is uncommon severe sight threatening complication of uveitis, more frequent in posterior uveitis. Hypoxia, release of vascular endothelial growth factor and other mediators seem to be involved in its pathogenesis. Multimodal imaging including the recent optical coherence tomography angiography greatly aid in diagnosis and management. Management of these neovascular membranes consists of anti-vascular growth factor agents, with or without concomitant anti-inflammatory and/or corticosteroid therapy. Besides effective eradication of inflammation in uveitis, the ideal therapeutic goal should include timely detection and treatment of inflammatory CNVM, as the ultimate visual outcome would depend on the control of both

RSC Advances ◽  
2020 ◽  
Vol 10 (46) ◽  
pp. 27288-27296
Author(s):  
Sima Singh ◽  
Arshid Numan ◽  
Yiqiang Zhan ◽  
Vijender Singh ◽  
Aftab Alam ◽  
...  

The vascular endothelial growth factor 165 (VEGF165) is a quintessential biomarker in cancers.


1998 ◽  
Vol 274 (5) ◽  
pp. H1620-H1626 ◽  
Author(s):  
Robert J. Tomanek ◽  
Kapildeo Lotun ◽  
Edward B. Clark ◽  
Padma R. Suvarna ◽  
Norman Hu

We tested the hypothesis that early vascularization of the embryonic heart is enhanced after bolus injections of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) into the vitelline vein before the onset of myocardial vasculogenesis (3.5 days, stage 21). Electron and light microscopy were utilized to obtain morphometric data. At stages 29 and 31, myocardial vessel volume or numerical density were higher in embryos injected with 50 ng bFGF than in the saline-injected controls. A VEGF injection increased vascular volume density at stage 29 and both volume and numerical density at stage 31. bFGF, but not VEGF, was associated with an enhancement of the sinusoidal system (spongy layer of the ventricle) at stage 29. This effect disappeared by stage 31. In conclusion, 1) enhancement of bFGF or VEGF before myocardial vascularization increases vascular growth, but the initial effect of bFGF is greater; 2) the effects of these growth factors on vascular volume and numerical density are temporally dependent; and 3) bFGF, in addition to its effects on the coronary vasculature, influences ventricular modeling by apparently acting on myocytes as well as endothelial cells.


2015 ◽  
Vol 129 (12) ◽  
pp. 1225-1236 ◽  
Author(s):  
Luigi Gnudi ◽  
Sara Benedetti ◽  
Adrian S. Woolf ◽  
David A Long

Kidney glomeruli ultrafilter blood to generate urine and they are dysfunctional in a variety of kidney diseases. There are two key vascular growth factor families implicated in glomerular biology and function, namely the vascular endothelial growth factors (VEGFs) and the angiopoietins (Angpt). We present examples showing not only how these molecules help generate and maintain healthy glomeruli but also how they drive disease when their expression is dysregulated. Finally, we review how manipulating VEGF and Angpt signalling may be used to treat glomerular disease.


2014 ◽  
Vol 42 (6) ◽  
pp. 1637-1642 ◽  
Author(s):  
Roberto Gianni-Barrera ◽  
Mariateresa Bartolomeo ◽  
Brigitte Vollmar ◽  
Valentin Djonov ◽  
Andrea Banfi

Therapeutic angiogenesis is an attractive strategy to treat patients suffering from ischaemic conditions and vascular endothelial growth factor-A (VEGF) is the master regulator of blood vessel growth. However, VEGF can induce either normal or aberrant angiogenesis depending on its dose localized in the microenvironment around each producing cell in vivo and on the balanced stimulation of platelet-derived growth factor-BB (PDGF-BB) signalling, responsible for pericyte recruitment. At the doses required to induce therapeutic benefit, VEGF causes new vascular growth essentially without sprouting, but rather through the alternative process of intussusception, or vascular splitting. In the present article, we briefly review the therapeutic implications of controlling VEGF dose on one hand and pericyte recruitment on the other, as well as the key features of intussusceptive angiogenesis and its regulation.


1995 ◽  
Vol 268 (6) ◽  
pp. C1362-C1368 ◽  
Author(s):  
J. M. Gleadle ◽  
B. L. Ebert ◽  
J. D. Firth ◽  
P. J. Ratcliffe

Recent work has indicated that oxygen-sensing mechanism(s) resembling those controlling erythropoietin production operate in many non-erythropoietin-producing cells. To pursue the implication that such a system might control other genes, we studied oxygen-regulated expression of mRNAs for vascular endothelial growth factor, platelet-derived growth factor (PDGF) A and B chains, placental growth factor (PLGF), and transforming growth factor in four different cell lines and compared the characteristics with those of erythropoietin regulation. Oxygen-regulated expression was demonstrated for each gene in at least one cell type. However, the response to hypoxia (1% oxygen) varied markedly, ranging from a 13-fold increase (PDGF-B in Hep G2 cells) to a 2-fold decrease (PLGF in the trophoblastic line BeWo). For each gene/cell combination, both the magnitude and direction of the response to hypoxia were mimicked by exposure to cobaltous ions or two different iron-chelating agents, desferrioxamine and hydroxypyridinones. These similarities with established characteristics of erythropoietin regulation indicate that a similar mechanism of oxygen sensing is operating on a variety of vascular growth factors, and they suggest that chelatable iron is closely involved in the mechanism.


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