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choroidal neovascularization/nicotina
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Nicotine promotes contribution of bone marrow-derived cells to experimental choroidal neovascularization in mice.
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Nicotine can increase size and severity of experimental choroidal neovascularization (CNV); however, the mechanism is uncertain. Recent studies demonstrated that the development of CNV involves the contribution of bone marrow-derived cells (BMCs). This study aims to investigate the effects and the
Alcohol and nicotine consumption exacerbates choroidal neovascularization by modulating the regulation of complement system.
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The objective of the present study was to investigate the effect of alcohol and nicotine consumption on the pathogenesis of choroidal neovascularization (CNV) in rats after laser-photocoagulation. Confocal microscopic analysis demonstrated an increase in CNV complex size in rats fed with alcohol
Mecamylamine suppresses Basal and nicotine-stimulated choroidal neovascularization.
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OBJECTIVE
Nicotinic acetylcholine receptors (nAChR) are best known for their role in neurotransmission, but they have recently been demonstrated on vascular endothelial cells. Acetylcholine is their endogenous ligand, but they are also stimulated by nicotine. By stimulating nAChR, nicotine promotes
Nicotine increases size and severity of experimental choroidal neovascularization.
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OBJECTIVE
Cigarette smoking is the strongest environmental risk factor for all forms of age-related macular degeneration (AMD). In the present study, the influence of nicotine on the severity of choroidal neovascularization (CNV) in a mouse model of neovascular AMD and its effects on vascular smooth
The effect of nicotine on anti-vascular endothelial growth factor therapy in a mouse model of neovascular age-related macular degeneration.
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OBJECTIVE
The purpose of this article is to evaluate the effect of nicotine on anti-vascular endothelial growth factor therapy in the treatment of neovascular age-related macular degeneration.
METHODS
One group of mice received nicotine in drinking water and the other group received water only.
Nicotine increases the VEGF/PEDF ratio in retinal pigment epithelium: a possible mechanism for CNV in passive smokers with AMD.
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OBJECTIVE
Cigarette smoking is the strongest environmental risk factor for wet age-related macular degeneration (AMD). Inappropriate expression of proangiogenic vascular endothelial growth factor (VEGF) and antiangiogenic pigment epithelium derived factor (PEDF) may cause choroidal
The genetic variant rs4073 A→T of the Interleukin-8 promoter region is associated with the earlier onset of exudative age-related macular degeneration.
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OBJECTIVE
To study the association of the single nucleotide polymorphism (SNP) rs4073 in the interleukin-8 (IL-8) promoter region with the diagnosis and age of onset of exudative age-related macular degeneration (AMD) in association with the known genetic risk factors for AMD and tobacco
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