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Abstract

Vascular Endothelial Growth Factor is a growth factor that plays a significant role in angiogenesis and vascular permeability. This paper dives into the development of diabetic retinopathy and age-related macular disease and focuses on the molecular pathway that VEGF goes through as the diseases progress. Diabetic retinopathy can progress from non-proliferative diabetic retinopathy into the more aggressive proliferative diabetic retinopathy through a series of molecular changes. In non-proliferative diabetic retinopathy hyperglycemia damages microvasculature and can lead leads to retinal vascular permeability, pericyte loss, microaneurysms, and acellular capillary formation. As the disease progresses, hypoxia leads to the production of VEGF which creates fragile blood vessels which is the major characteristic of proliferative diabetic retinopathy. The new vessels are prone to hemorrhages, fluid leakage, and the scarring can lead to vision loss. This is further emphasized by the vitreous gel adhering to the retina which leading to significant complications. Proliferative diabetic retinopathy is characterized by neovascularization and ultimately leads to retinal detachment, vitreous hemorrhaging, and finally total vision loss. Diabetic retinopathy and age-related macular degeneration have similar pathophysiological mechanisms such as oxidative stress, leakage and fluid accumulation, and the function of VEGF leading to oxidative stress. Anti-VEGF treatments have been shown to prevent the progression of these diseases and improve the lives of these patients. This paper analyzes the specific molecular role that VEGF follows and reveals the many pathophysiological mechanisms and its impact on vision and disease progression. It also underscores the significance of VEGF in clinical practice, providing the audience with provocative, trustworthy, and comprehensive information.

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VEGF in Diabetic Retinopathy and Age-Related Macular Degeneration

Vascular Endothelial Growth Factor is a growth factor that plays a significant role in angiogenesis and vascular permeability. This paper dives into the development of diabetic retinopathy and age-related macular disease and focuses on the molecular pathway that VEGF goes through as the diseases progress. Diabetic retinopathy can progress from non-proliferative diabetic retinopathy into the more aggressive proliferative diabetic retinopathy through a series of molecular changes. In non-proliferative diabetic retinopathy hyperglycemia damages microvasculature and can lead leads to retinal vascular permeability, pericyte loss, microaneurysms, and acellular capillary formation. As the disease progresses, hypoxia leads to the production of VEGF which creates fragile blood vessels which is the major characteristic of proliferative diabetic retinopathy. The new vessels are prone to hemorrhages, fluid leakage, and the scarring can lead to vision loss. This is further emphasized by the vitreous gel adhering to the retina which leading to significant complications. Proliferative diabetic retinopathy is characterized by neovascularization and ultimately leads to retinal detachment, vitreous hemorrhaging, and finally total vision loss. Diabetic retinopathy and age-related macular degeneration have similar pathophysiological mechanisms such as oxidative stress, leakage and fluid accumulation, and the function of VEGF leading to oxidative stress. Anti-VEGF treatments have been shown to prevent the progression of these diseases and improve the lives of these patients. This paper analyzes the specific molecular role that VEGF follows and reveals the many pathophysiological mechanisms and its impact on vision and disease progression. It also underscores the significance of VEGF in clinical practice, providing the audience with provocative, trustworthy, and comprehensive information.

 

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