Vascular endothelial growth factor (VEGF) is an important regulator of angiogenesis and a target for inhibition therapy in wet age-related macular degeneration (AMD).
Inhibition of vascular endothelial growth factor (VEGF) has become the standard of care for patients presenting with wet age-related macular degeneration.
Moreover, the presence of anti-angiogenic forms of VEGF may explain the disappointing efficacy of anti-VEGF therapies on the overall survival of patients with different forms of cancers and with wet age-related macular degeneration.
QUANTITATIVE ANALYSIS OF PIGMENT EPITHELIAL DETACHMENT RESPONSE TO DIFFERENT ANTI-VASCULAR ENDOTHELIAL GROWTH FACTOR AGENTS IN WET AGE-RELATED MACULAR DEGENERATION.
Dysregulation of RPE- and podocyte-derived VEGF is associated with neovascularization in wet age-related macular degeneration (ARMD), choriocapillaris degeneration, and glomerular thrombotic microangiopathy (TMA).
To investigate detailed patient experiences specific to receiving vascular endothelial growth factor inhibitors (anti-VEGF) for wet age-related macular degeneration (wAMD), and to acquire a snapshot of the frequency of clinically significant levels of depression, anxiety, and posttraumatic stress among patients and levels of burden in patients' carers.
Angiogenesis, in which vascular endothelial growth factor receptor (VEGFR) 2 plays an essential role, is associated with a variety of human diseases including proliferative diabetic retinopathy and wet age-related macular degeneration.
The standard-of-care therapeutics for the treatment of ocular neovascular diseases like wet age-related macular degeneration (AMD) are biologics targeting vascular endothelial growth factor signaling.
To develop a generative mathematical model of wet age-related macular degeneration (AMD) and model the impact of injections of anti-vascular endothelial growth factor to virtual patients with the condition.
Vascular endothelial growth factor (VEGF) is a key mediator in the development and progression of choroidal neovascularization (CNV) in patients with wet age-related macular degeneration (AMD).
To identify disease-specific cytokine profile differences in the aqueous humor (AH) (other than the vascular endothelial growth factor) between patients with dry and treated wet age-related macular degeneration (AMD) and healthy controls.
Sasaki and colleagues [1] (JCI Insight 2018;3,e96902) identified the leukocyte inflammatory lipid mediator leukotriene B4 (LTB4)/LTB4 receptor 1 receptor-signaling axis in M2 macrophages as a causal pathway for the vascular endothelial growth factor-dependent pathological neovascularization in a mouse model that mimics wet age-related macular degeneration.
The intravitreous injection of therapeutic proteins that neutralize vascular endothelial growth factor (VEGF) family members is efficient to reduce macular edema associated with wet age-related macular degeneration (AMD), retinal vein occlusion (RVO) and diabetic retinopathy (DR).
<b>Areas covered</b>: VEGF (vascular endothelial growth factor) is a hypoxia-induced growth factor promoting neoangiogenesis, which has been correlated to the pathogenesis of w-AMD.
Priority options of anti-vascular endothelial growth factor agents in wet age-related macular degeneration under the National Health Insurance Program.
The pathophysiological mechanisms for dry and wet age-related macular degeneration (AMD) involve oxidative stress and increased VEGF release and expression.
Brolucizumab (Beovu<sup>®</sup>) is a low molecular weight, single-chain antibody fragment vascular endothelial growth factor (VEGF) inhibitor being developed by Novartis for the treatment of exudative (wet) age-related macular degeneration (AMD), diabetic macular oedema and macular oedema secondary to retinal vein occlusion.