hVEGFA-TG Mouse

The Vascular Endothelial Growth Factor (VEGF) family is a group of particular endothelial growth factors intimately associated with angiogenesis. These factors promote increased vascular permeability, extracellular matrix degeneration, vascular endothelial cell migration and proliferation, and are capable of stimulating angiogenesis and increasing the permeability of existing vessels. As such, they play a pivotal role in normal vascular development and wound healing. The VEGF family comprises VEGFA, VEGFB, VEGFC, VEGFD, VEGFE, and PLGF^[1]. Of these, VEGFA is the most commonly targeted in research related to neovascular ophthalmic diseases due to its crucial role in the proliferation, migration, and formation of endothelial cell microvessels^[2]. Overexpression of VEGFA in the eye can result in abnormal vascular growth and leakage, leading to various ophthalmic diseases such as Age-Related Macular Degeneration (AMD), Diabetic Retinopathy (DR), and corneal neovascularization^[2-3].

The hVEGFA-TG mouse is a transgenic model generated by Cyagen. In this model, the expression of human VEGFA CDS is driven by the bovine rhodopsin promoter, allowing for specific overexpression of the human VEGFA gene in the retina without affecting the expression of the endogenous VEGFA gene. This model exhibits clear retinal and choroidal vascular lesions while maintaining complete eye structure and can naturally develop diseases. Anti-VEGF drugs such as Aflibercept^[4] have been evaluated for efficacy in this mouse model, demonstrating that Aflibercept can target and suppress VEGF expression, thereby alleviating retinal vascular lesions. As such, this model is well-suited for drug evaluation and mechanism research related to neovascular ophthalmic diseases.