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).
The pathophysiological mechanisms for dry and wet age-related macular degeneration (AMD) involve oxidative stress and increased VEGF release and expression.
Priority options of anti-vascular endothelial growth factor agents in wet age-related macular degeneration under the National Health Insurance Program.
<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.
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.
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.
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).
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 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.
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.
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.
QUANTITATIVE ANALYSIS OF PIGMENT EPITHELIAL DETACHMENT RESPONSE TO DIFFERENT ANTI-VASCULAR ENDOTHELIAL GROWTH FACTOR AGENTS IN WET AGE-RELATED MACULAR DEGENERATION.
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.
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).
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.
Inhibition of vascular endothelial growth factor (VEGF) has become the standard of care for patients presenting with wet age-related macular degeneration.
Vascular endothelial growth factor (VEGF) is an important regulator of angiogenesis and a target for inhibition therapy in wet age-related macular degeneration (AMD).